Apoptosis In Lung Cancer Cells Research Articles

Interferon regulatory factor-1 regulates cisplatin-induced apoptosis and autophagy in A549 lung cancer cells

This study aimed to investigate the expression and function of interferon regulatory factor-1 (IRF-1) in non-small cell lung cancer (NSCLC). IRF-1 expression and its prognostic value were investigated through bioinformatic analysis. The protein expression levels of IRF-1, cleaved caspase 3, and LC3-I/II were analyzed by western blotting. A lentiviral vector was used to overexpress or knockdown IRF-1 in vitro. Mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) were analyzed by JC-1 and DCFH-DA staining, respectively. ATP, SOD, MDA, cell viability, LDH release, and caspase 3 activity were evaluated using commercial kits. Compared to the levels in normal tissues, IRF-1 expression was significantly lower in lung cancer tissues and was a prognostic factor for NSCLC. Cisplatin treatment-induced IRF-1 activation, ROS production, ATP depletion, SOD consumption, and MDA accumulation in A549 lung cancer cells. IRF-1 overexpression promoted mitochondrial depolarization, oxidative stress, and apoptotic cell death and inhibited autophagy in A549 cells, and these effects could be reversed by IRF-1 knockdown. These data suggest that IRF-1 regulates apoptosis, autophagy and oxidative stress, which might be served as a potential target for increasing chemotherapy sensitivity of lung cancer.

LncCDH5-3:3 Regulates Apoptosis, Proliferation, and Aggressiveness in Human Lung Cancer Cells.

(1) Lung cancer (both small cell and non-small cell) is the leading cause of new deaths associated with cancers globally in men and women. Long noncoding RNAs (lncRNAs) are associated with tumorigenesis in different types of tumors, including lung cancer. Herein, we discuss: (1) An examination of the expression profile of lncCDH5-3:3 in non-small cell lung cancer (NSCLC), and an evaluation of its functional role in lung cancer development and progression using in vitro models; (2) A quantitative real-time polymerase chain reaction assay that confirms lncCDH5-3:3 expression in tumor samples resected from 20 NSCLC patients, and that shows its statistically higher expression levels at stage III NSCLC, compared to stages I and II. Moreover, knockout (KO) and overexpression, as well as molecular and biochemical techniques, were used to investigate the biological functions of lncCDH5-3:3 in NSCLC cells, with a focus on the cells’ proliferation and migration; (3) The finding that lncCDH5-3:3 silencing promotes apoptosis and probably regulates the cell cycle and E-cadherin expression in adenocarcinoma cell lines. In comparison, lncCDH5-3:3 overexpression increases the expression levels of proliferation and epithelial-to-mesenchymal transition markers, such as EpCAM, Akt, and ERK1/2; however, at the same time, it also stimulates the expression of E-cadherin, which conversely inhibits the mobility capabilities of lung cancer cells; (4) The results of this study, which provide important insights into the role of lncRNAs in lung cancer. Our study shows that lncCDH5-3:3 affects important features of lung cancer cells, such as their viability and motility. The results support the idea that lncCDH5-3:3 is probably involved in the oncogenesis of NSCLC through the regulation of apoptosis and tumor cell metastasis formation.

The effect and mechanisms of melatonin on the proliferation and apoptosis of lung cancer cells

ABSTRACT The aim of the present study was to observe the effects and mechianisms of melatonin on the proliferation and apoptosis of lung cancer (LC) cells. A549 cells were treated with a concentration gradient (0–100 μM) of melatonin for 24 hours, and cell viability was detected by XTT ((2,3-Bis-(2-methoxy-4-nitro-5-sulfophenyl) −2H-tetrazolium-5-carboxanilide)) colorimetry. Melatonin with a concentration of 50 μM was selected to interact with the LC cells for ten days, and then a colony formation assay was used to detect the proliferation of the LC cells. TUNEL (Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling) staining was used to evaluate the amount of apoptosis in the two groups. Finally, Western blotting was used to detect the expression levels of related proteins in the p38MAP (mitogen-activated protein) signaling pathway. Meanwhile, another experiment, CCK-8 cell proliferation test, was conducted to detect the OD540 absorbance of LC cells at 24, 48, 72, and 96 hours. Melatonin inhibited the proliferation of LC cells in a concentration-dependent (5–100 μM) manner (P < 0.05), and inhibited the proliferation of LC cells in a time-dependent (0–96 hour) manner (P < 0.05). Melatonin (50 μM) could significantly inhibit the colony formation ability of LC cells (P < 0.05). The ratio of LC cells in the G0/G1 phase in the melatonin group increased, while the ratio of cells in the G2/M and S phase was significantly reduced (P < 0.05). Melatonin significantly promoted the apoptosis of LC cells (P < 0.05) and activate the phosphorylation of p38 (P < 0.05).

XIST/miR-34a-5p/PDL1 axis regulated the development of lung cancer cells and the immune function of CD8+ T cells

Purpose Long non-coding RNA (lncRNA) XIST has been shown to be involved in the immune escape of breast cancer, but it is unclear whether it is involved in the immune escape of lung cancer, so it will be discussed in this study. Methods XIST and miR-34a-5p expression in lung cancer tissues and cells were detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The targeting relationship between miR-34a-5p and XIST/programmed cell death receptor ligand 1 (PDL1) was predicted by bioinformatics website and verified by dual-luciferase report experiment. After co-transfection with XIST specific short hairpin RNA (sh-XIST) and miR-34a-5p inhibitors, the changes in PDL1 expression, and cell biological behavior were detected by qRT-PCR, cell counting kit 8, flow cytometry, and Transwell experiments. Similarly, after co-transfection of PDL1 specific small interfering RNA (siPDL1) and miR-34a-5p inhibitors, the changes in cell biological behavior were detected again. After CD8+ T cells were co-cultured with lung cancer cells transfected with sh-XIST and miR-34a-5p inhibitors, the expression of cytokines and immunosuppressive molecules was detected by western blot and enzyme-linked immunosorbent assay (ELISA). Results XIST was up-regulated in lung cancer tissues, while miR-34a-5p was the opposite. XIST up-regulated the expression of PDL1 by targeting miR-34a-5p, thereby affecting the viability, apoptosis, migration, and invasion of lung cancer cells. In the co-culture system, XIST targeted miR-34a-5p to inhibit cytokines secretion and promote the expression of immunosuppressive molecules. Conclusions XIST/miR-34a-5p/PDL1 axis was involved in the malignant biological behavior of lung cancer cells and the immune function of CD8+ T cells.

Novel imidazo[1,2-a]pyridine derivatives induce apoptosis and cell cycle arrest in non-small cell lung cancer by activating NADPH oxidase mediated oxidative stress

AimsImidazo[1,2-a]pyridine-based analogues have recently gained significant interest because of their wide spectrum of biological activities including anti-cancer potential, however the development of targeted therapeutic candidates against non-small cell lung cancer (NSCLC) is of utmost need due to its high prevalence and poor prognosis. Herein, we have aimed to synthesized novel imidazo [1,2-a] pyridine derivatives (IMPA) by coupling with 2-amino-4H-pyran to enhance bioactivity against NSCLC. Main methodsWe have designed and synthesized a series of fifteen novel imidazo [1,2-a] pyridine derivatives through molecular hybridization and studied their anti-cancer activity against in-vitro lung adenocarcinoma and 3D multicellular lung tumor spheroids. Key findingsIMPA-2, IMPA-5, IMPA-6, IMPA-8, and IMPA-12 markedly induced cytotoxicity by notably increased NADPH oxidase (NOX) activity, which results in the induction of ROS-mediated apoptosis in A549 lung cancer cells. It caused impairment of mitochondrial membrane potential by increasing pro-apoptotic BAX, and BAK1 expressions, and decreasing anti-apoptotic BCL2 expression, along with the induction of caspase-9/3 activation, however, these attributes were compromised in presence of N-acetyl-L-cysteine (NAC), a free radical scavenger. Increased ROS production by IMPAs also promotes p53 mediated cell cycle arrest through the inactivation of p38MAPK. Reduction of tumor size in IMPAs-treated 3D multicellular lung tumor spheroids gave further validation. SignificanceBeside cytotoxicity, IMPAs also inhibit lung cancer cell invasion and migration, suggesting their applicability in metastatic lung cancer. Therefore, IMPA derivatives could be used as potential anti-cancer agents in treating non-small cell lung cancer.

Paeonol enhances TRAIL-induced apoptosis of human lung cancer cells by upregulating death receptors-4 and 5 via ROS-JNK/ERK-CHOP signaling

&#x0D; &#x0D; &#x0D; &#x0D; Purpose: To study the anti-proliferative potential of paeonol against lung cancer cells, and investigate its mechanism of action.&#x0D; Methods: Cell viability after paeonol treatment was determined with 3-(4,5-dimethylthiazol-2yl)2,5- diphenyltetrazolium bromide (MTT) assay, while paeonol- and TRAIL-mediated apoptosis was assayed using flow cytometry. Western blotting was used to assay the protein expression levels of phosphorylated JNK and ERK1/2, as well as protein expressions of pro-apoptotic factors/death receptors. 2′,7′-Dichlorodihydrofluorescein diacetate (H2DCFDA) staining and flow cytometry were used to monitor paeonol-induced reactive oxygen species (ROS) in the cells.&#x0D; Results: Paeonol treatment markedly reduced the proliferations of H1975 and BGC823 cells (p &lt; 0.05). In H1975 and BGC823 cells, paeonol/TRAIL combination increased apoptosis to 88.43 and 87.21 %, respectively (p &lt; 0.05). The levels of death receptor 4 (DR4) and death receptor 5 (DR5) were increased significantly by paeonol, relative to the control (p &lt; 0.05). Paeonol also reduced the levels of decoy receptor-1 (DcR1) and decoy receptor-2 (DcR2), and increased the expression of CHOP (p &lt; 0.05). The protein expression levels of survivin, Bcl-2, cFLIP and Bcl-xL were decreased, while protein levels of caspase3, caspase-8 and caspase-9 were upregulated by paeonol. Moreover, paeonol significantly upregulated p-ERK and p-JNK in H1975 and BGC823 cells, and also increased ROS levels, when compared to control (p &lt; 0.05).&#x0D; Conclusion: Paeonol exerts anti-proliferative potential on lung cancer cells through upregulation of death receptors, activation of JNK/ERK-CHOP pathway and generation of ROS. Therefore, paeonol has a therapeutic potential for the management of lung cancer.&#x0D; &#x0D; &#x0D; &#x0D;

Dexmedetomidine Associated Lung Cancer Proliferation and Tumor Growth is Prevented by β-Caryophyllene: Role of AMPK Activation and PGC-1α/TFAM Over Expression

Background: Dexmedetomidine has been reported to induce anti-apoptotic effects and metastatic progression in lung cancer. In the current investigation, the effect of β-Caryophyllene on dexmedetomidine induced cell proliferation and apoptosis of lung cancer cells and tumor growth in mice was studied. Methods: A549 cell line was cultured with either dexmedetomidine alone or together with β-Caryophyllene for 24 h and analysed for cell proliferation with MTT assay. ELISA based kit was used to determine apoptotic DNA fragmentation. Western blotting was used to determine expression levels of target proteins. The induction of experimental lung tumor in rat model was achieved through the injection of A549 tumor cells subcutaneously into the middle left side of the mice after anesthetization with pentobarbital (35 mg/kg) at 2.8 × 106 cells in 400 μl of PBS. Result: We found that β-Caryophyllene exerts the anti-proliferative effects on A549 cells. Furthermore, β-Caryophyllene significantly prevents apoptotic cell death and causes up-regulation of PGC-1α and TFAM compared to dexmedetomidine treated cells. We observed that β-Caryophyllene suppressed tumor development in mice significantly compared to dexmedetomidine treated group without changing body weight.

Amygdalin Induced Mitochondria-Mediated Apoptosis of Lung Cancer Cells via Regulating NF[Formula: see text]B-1/NF[Formula: see text]B Signaling Cascade in Vitro and in Vivo.

Lung cancer is the most commonly diagnosed cancer and the leading cause of cancer death worldwide. Amygdalin, a natural compound commonly distributed in plants of the Rosaceae species, owns anticancer activity, less side effects, wide source, and relatively low price. Although the apoptosis is a central process activated by amygdalin in cancer cells, the underlying molecular mechanisms through which amygdalin induces the apoptosis of lung cancer cells remain poorly understood. In this research work, amygdalin could suppress the proliferation of lung cancer A549 and PC9 cells by CCK8 assay. Amygdalin significantly promoted the apoptosis of lung cancer A549 and PC9 cells stained with Annexin V-FITC/PI by flow cytometry assay. Furthermore, amygdalin dose-dependently decreased the mitochondrial membrane potential (MMP) with JC-1 dye by flow cytometry. To investigate the underlying molecular mechanisms through which amygdalin induced mitochondria-mediated apoptosis of cancer cells, the differentially-expressed genes with a fold change >2.0 and p < 0.05 were acquired from the cDNA microarray analysis. The results of qRT-PCR further confirmed that the differentially-expressed level of the NF[Formula: see text]B-1 gene was most obviously enhanced in lung cancer cells treated with amygdalin. The results of immunofluorescence staining, Western blotting and siRNA knockdown indicated that amygdalin induced mitochondria-mediated apoptosis of lung cancer cells via enhancing the expression of NF[Formula: see text]B-1 and inactivating NF[Formula: see text]B signaling cascade and further changing the expressions of proteins (Bax, Bcl-2, cytochrome C, caspase 9, caspase 3 and PARP) related to apoptosis, which were further checked by in vivo study of the lung cancer cell xenograft mice model accompanying with immunohistochemical staining and TUNEL staining. Our results indicated that amygdalin might be a potential activator of NF[Formula: see text]B-1, which sheds more light on the molecular mechanism of anticancer effects of amygdalin. These results highlighted amygdalin as a potential therapeutic anticancer agent, which warrants its development as a therapy for lung cancer.

Expression of concern: LncRNA CASC2 inhibits autophagy and promotes apoptosis in non-small cell lung cancer cells via regulating the miR-214/TRIM16 axis.

Expression of concern for ‘LncRNA CASC2 inhibits autophagy and promotes apoptosis in non-small cell lung cancer cells via regulating the miR-214/TRIM16 axis’ by Qian Li et al., RSC Adv., 2018, 8, 40846–40855, DOI: 10.1039/c8ra09573f.

Vorinostat enhances the therapeutic potential of Erlotinib via MAPK in lung cancer cells

BackgroundLung cancer is the second most common cancer in both men and women, with an estimated 235,760 new cases and 131,880 deaths in 2021 in the US. Despite the modern therapies being available such as radiotherapy and chemotherapy, death rates are still increasing. Erlotinib (ERL) is one of the treatment options for lung cancer, although the probability for the patients to develop resistance to ERL constrains its reliability. The aim of the present study is to assess the synergetic effect of combining ERL with vorinostat (SAHA) on the progression of lung cancer cells. ResultsAdenocarcinoma alveolar basal epithelial cells (A549) were treated with either ERL, SAHA as mono drugs or with the combination of them for 24 h. Cytotoxicity assay and cell cycle analysis along with apoptosis detection were investigated. The expression profile of CDH1, TGF1, and MAPK was also assessed. Results showed an elevation in the apoptosis level in all treatments compared to WISH; the normal human amnion-derived cells. Furthermore, the treatments caused the cell cycle to arrest at G2/M, indicating its cytotoxic activity. ConclusionThe combination of SAHA and ERL significantly increased the level of apoptosis in lung cancer cells. Meanwhile, this combination treatment downregulated MAPK compared to the mono drugs and the control cells, suggesting the potential role of MAPK in regulating apoptosis and cell cycle machinery in lung cancer.

Bound Polyphenols Extracted From Etlingera Linguiformis Arrests Cell Cycle And Induce Apoptosis In Lung Cancer Cells

Lung cancer (LC) is India's biggest cause of mortality and rising lung cancer deaths get a worldwide concern. Cost effective, suitable drugs with minimal side effects are the researcher's biggest problems while dealing with lung cancer. This raises the need for scientists to find biocompatible, affordable medications that are reachable to the masses of underdeveloped countries like India. Tribes rely on abundant biodiversity of food, housing, and wellness, according to traditional awareness with this background, Etlingera linguiformis (CAN) leaves were chosen for their bioactive components and empirical use. The antitumor efficiency of the hydro-alcoholic extract was studied utilising in-vitro cell culture on lung cancer cells, A549. CAN bound polyphenolic fraction was evaluated for the further anticancer potential and was tested for cell viability, apoptosis by Acridine Orange (AO), Intracellular Reactive Oxygen Species (ROS) generation, cell cycle analysis, cell proliferation. The findings demonstrated a dose as well as time-dependent decrease in cancer cell viability and other analysis relative to controls.

LINC01204 Negatively Regulates the Effect of MiR-214 on Lung Cancer Cell Apoptosis, Migration, Invasion and Radio-sensitivity

LINC01204 Negatively Regulates the Effect of MiR-214 on Lung Cancer Cell Apoptosis, Migration, Invasion and Radio-sensitivity

Solanum Procumbens-Derived Zinc Oxide Nanoparticles Suppress Lung Cancer In Vitro through Elevation of ROS.

Lung cancer is one of the cancers with high mortality rate. The current therapeutic regimens have only limited success rate. The current work highlights the potential of Solanum procumbens-derived zinc oxide nanoparticle (SP-ZnONP)-induced apoptosis in A549 lung cancer cells. Synthesized nanoparticles were confirmed by UV-Vis spectrophotometry, X-ray diffraction (XRD), dynamic light scattering analysis (DLS), scanning electron microscopy (SEM), Fourier transform infrared (FT-IR), and photoluminescence analysis. Lactate dehydrogenase (LDH), cytotoxicity, and cell viability assays revealed that the SP-ZnONP caused the cell death and the inhibition concentration (IC50) was calculated to be 61.28 μg/mL. Treatment with SP-ZnONPs caused morphological alterations in cells, such as rounding, which may have been caused by the substance's impact on integrins. Acridine orange/ethidium bromide dual staining revealed that the cells undergo apoptosis in a dose-dependent manner, which indicates the cell death. Furthermore, reactive oxygen species (ROS) were examined and it was shown that the nanoparticles elevated ROS levels, which led to lipid peroxidation. In short, the SP-ZnONPs increase the level of ROS, which in turn causes lipid peroxidation results in apoptosis. On the other hand, the SP-ZnONPs decrease nitric oxide level in A549 cells in a dose-dependent manner, which also supports the apoptosis. In conclusion, SP-ZnONPs would become a promising treatment option for lung cancer.

Targeting the anti-apoptotic Bcl-2 family proteins: machine learning virtual screening and biological evaluation of new small molecules.

Bcl-2 family anti-apoptotic proteins are overexpressed in several hematological and solid tumors, and contribute to tumor formation, progression, and resistance to therapy. They represent a promising therapeutic avenue to explore for cancer treatment. Venetoclax, a Bcl-2 inhibitor is currently used for hematological malignancies or is undergoing clinical trials for either hematological or solid tumors. Despite these progresses, ongoing efforts are focusing on the identification and development of new molecules targeting Bcl-2 protein and/or other family members.Methods: Machine learning guided virtual screening followed by surface plasmon resonance, molecular docking and pharmacokinetic analyses were performed to identify new inhibitors of anti-apoptotic members of Bcl-2 family and their pharmacokinetic profile. The sensitivity of cancer cells from different origin to the identified compounds was evaluated both in in vitro (cell survival, apoptosis, autophagy) and in vivo (tumor growth in nude mice) preclinical models.Results: IS20 and IS21 were identified as potential new lead compounds able to bind Bcl-2, Bcl-xL and Mcl-1 recombinant proteins. Molecular docking investigation indicated IS20 and IS21 could bind into the Beclin-1 BH3 binding site of wild type Bcl-2, Bcl-xL and Mcl-1 proteins. In particular, although the IS21 docked conformation did not show a unique binding mode, it clearly showed its ability in flexibly adapting to either BH3 binding sites. Moreover, both IS20 and IS21 reduced cell viability, clonogenic ability and tumor sphere formation, and induced apoptosis in leukemic, melanoma and lung cancer cells. Autophagosome formation and maturation assays demonstrated induction of autophagic flux after treatment with IS20 or IS21. Experiments with z-VAD-fmk, a pan-caspase inhibitor, and chloroquine, a late-stage autophagy inhibitor, demonstrated the ability of the two compounds to promote apoptosis by autophagy. IS21 also reduced in vivo tumor growth of both human leukemia and melanoma models.Conclusion: Virtual screening coupled with in vitro and in vivo experimental data led to the identification of two new promising inhibitors of anti-apoptotic proteins with good efficacy in the binding to recombinant Bcl-2, Bcl-xL and Mcl-1 proteins, and against different tumor histotypes.

Evaluation of Anti-Cancer Activity of Gryllus bimaculatus Water Extract on Non-Small Cancer Lung Cell via Apoptosis.

Gryllus bimaculatus, traditionally used in oriental medicine, demonstrates functional and pharmacological potential through demonstrating immunomodulatory, hepato-protective properties, anti-inflammatory, antioxidant, and neuroprotective effects. In this study, we examined the effect of G. bimaculatus on cell proliferation and apoptosis in lung cancer cells. This is the first study to examine the anti-cancer effects of G. bimaculatus extracts on non-small cell lung cancer. Frozen G. bimaculatus was obtained, homogenized, and dissolved in distilled water. Using a freeze dryer, samples were concentrated until almost all the water was removed, and extracts were diluted in solutions of phosphate buffered saline. Anti-cancer effects of extracts on human non-small cancer lung cells were estimated based on cell cytotoxicity, western blot, and flow cytometry, using lipopolysaccharides as a positive control. H460 and A549 human non-small cell cancer lung cells were treated with G. bimaculatus water extracts of various concentrations, with lipopolysaccharide used as a pos-itive control. The results showed that treatment with the extract for 24 or 48 h inhibited H460 proliferation, demonstrated by reduced cell numbers with morphological changes. Furthermore, flow cytometry analysis demonstrated that the extracts induced cell death on H460. However, extracts did not show cytotoxic effects on A549 cells. In conclusion, the extract induced apoptosis of lung cancer cells, possibly via caspase, Bcl-2 family signaling pathways. Therefore, G. bimaculatus water extracts are safe and efficient natural materials that may have great potential in the treatment of lung cancer.

Cucurbitacin B regulates lung cancer cell proliferation and apoptosis via inhibiting the IL-6/STAT3 pathway through the lncRNA XIST/miR-let-7c axis

Context Lung cancer, the most common type of cancer, has a high mortality rate. Cucurbitacin B (CuB), a natural compound extracted from Cucurbitaceae plants, has antitumor effects. Objective We investigated the role of CuB on lung cancer and its potential mechanisms. Materials and methods A549 cells were treated with 0.1, 0.3, 0.6, and 0.9 μM CuB for 12, 24, and 48 h or untreated. Gene and protein levels were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. Enzyme-linked immunosorbent assay (ELISA) detected inflammatory factors levels (TNF-α and IL-10). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and colony formation assays measured cell viability, apoptosis, and proliferation. The interaction between miR-let-7c and long non-coding RNA X inactive-specific transcript (XIST) or interleukin-6 (IL-6) was verified by dual-luciferase reporter assays. Results CuB treatment inhibited the proliferation of lung cancer cells and promoted cell apoptosis, and increased the expression of Bax and cleaved caspase3, decreased cyclin B1 and Bcl-2 expression. CuB suppressed XIST and IL-6 expression, and enhanced miR-let-7c expression. XIST silencing enhanced the inhibitory effect of CuB on cell proliferation and the promotion effect on apoptosis via upregulating miR-let-7c. Moreover, XIST targeted miR-let-7c to activate the IL-6/STAT axis. MiR-let-7c overexpression enhanced the regulatory effect of CuB on proliferation and apoptosis via suppressing the IL-6/STAT3 pathway. Discussion and conclusion CuB regulated cell proliferation and apoptosis by inhibiting the XIST/miR-let-7c/IL-6/STAT3 axis in lung cancer. These findings indicate CuB may have the possibility of clinical application in lung cancer treatment.

Evaluation of Cytotoxic Potential of Digera muricata Leaf Extract on Lung Cancer Cell Line

Lung cancer is the second most frequent cancer, accounting for one out of every five male cancers and one out of every nine female cancers. Treatment for lung cancer is determined by the disease's cell type, the extent to which it has spread, and the patient's overall health. It is common knowledge that tumours impart resistance to chemotherapeutic medicines or radiation in part owing to apoptotic pathway dysfunction in cancer cells. Digera muricata (D.muricata) has been used as medicinal remedies for various ailments due to its antioxidant, anti-inflammatory, anti-bacterial, anti-tumor activity. The objective of the study was to examine the cytotoxic activity of ethanolic leaf extract of D.muricata on lung cancer cell lines. The cytotoxic potency of D.muricata leaf extract was carried out by MTT assay against the lung cancer cell line (A549). Different concentrations of D.muricata ethanolic leaf extract (25-150µg/ml) were treated for 24h. Furthermore, the morphological changes were analysed using phase contrast microscopy. Pro-apoptotic and nuclear morphological changes in D. muricata ethanolic leaf extract treated cells were examined using DAPI staining. The ethanolic leaf extract of D.muricata showed the dose dependent cytotoxic potency against the A549 cell line which confirmed with greater morphological changes upon 24 hrs treatment. The MTT assay clearly showed that the D.muricata treatment has significantly reduced the cell viability when the concentration was increased for 24hrs. We observed IC-50 dose at 50 μg/ml concentration. DAPI staining clearly showed condensed chromatin and fragmented nuclei in treated lung cancer cells. All these results clearly showed that ethanolic extract of D. muricata treatment significantly inhibited the cell proliferation and induced apoptosis in lung cancer cells.

Evaluation of Anti-Cancer Activity of Saraca asoca Flower Extract against Lung Cancer Cell Line

Lung cancer is the second most common type of cancer, affecting one out of every five men and one out of every nine women. Lung cancer treatment is dictated by the cell type of the cancer, the amount to which it has spread, and the patient's overall condition. It is well known that cancer cells, in part due to apoptotic pathway malfunction, confer resistance to chemotherapy drugs or radiation. Saraca Asoca (S. asoca) has been used as medicinal remedies for various ailments due to its antioxidant, anti-inflammatory, anti-bacterial, anti-tumor activity. The objective of the study was to evaluate the anti-cancer activity of S. asoca flower extract against lung cancer cell line. The cytotoxic effect of S. asoca flower extract was carried out by cell viability assay against the lung cell line (A549). Different concentrations of S. asoca flower ethanolic extract (20-120µg/ml) were treated for 24h. Furthermore, the morphological changes were analysed using inverted microscopy. The nuclear morphology of S. asoca flower ethanolic extract treated lung cancer was analyzed by DAPI staining. The cell viability assay clearly showed that the extract of S. asoca flower treatment has significantly reduced the lung cancer cell viability in a dose dependent manner. We observed the IC50 dose at 60 μg/ml concentration. The DAPI staining results showed increased apoptotic cells with condensed chromatin and nuclear fragmentation in ethanolic extract of S. asoca flower treatment in lung cancer cells. The present study shows ethanolic extract of S. asoca flower treatment inhibits cell growth and induces the apoptosis in lung cancer cells. Further research is needed to find out the active compounds and understand the mechanisms of anti-cancer effects of S. asoca flower.

Investigating Cytotoxic Effect and Molecular Mechanisms of Quinoa Seed Extract Against Human Lung Cancer Cell Line

Background: Lung cancer is one of the most common leading causes of mortality and morbidity worldwide. Despite recent advances in therapeutic approaches, common methods are not fully effective. Thus, researchers are looking for some novel complementary agents to improve the effectiveness of therapies. Emerging evidence has shown the antitumor activity of several natural components such as quinoa seed extracts in various types of cancer. Objectives: Hence, this study was conducted to evaluate the antiproliferation and anti-apoptotic activity of quinoa on the A549 lung cancer cell line. Methods: The cell viability of A549 cells treated with quinoa was detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression levels of BAX and BCL2 as apoptosis-related genes were assessed using real-time polymerase chain reaction (PCR). Finally, the statistical analysis was performed using GraphPad Prism version 7. Results: Our findings demonstrated that the cell viability decreased in a concentration and time-dependent manner. Also, treating A549 cells with doses of 1.60 and 1.92 mg/mL of quinoa seed extracts could increase BAX and decrease BCL2 expression levels (P &lt; 0.05). However, the higher dose (1.92 mg/mL) was significantly effective. Conclusions: According to this study, quinoa seed extract could induce apoptosis in lung cancer cells (A549) throughout the increased ratio of BAX/BCL2. However, further investigations are required to confirm the results.

LINC00839/miR-519d-3p/JMJD6 axis modulated cell viability, apoptosis, migration and invasiveness of lung cancer cells.

Long noncoding RNAs are associated with progressions of lung cancer. LINC00839 has been dysregulated in osteosarcoma, breast cancer and lung cancer (LC). As an upregulated lncRNA, the roles of LINC00839 in lung cancer remain unclear. RNA expressions of LINC00839, miR-519d-3p and JMJD6 were assessed using RT-qPCR and JMJD6 protein expression were analyzed through Western blot. Meanwhile, viabilities of A549 and H460 LC cells transfected by siNC, siLINC00839, oeNC, oeLINC00839, NC mimics, miR-519d-3p mimics and oeLINC00839 with siJMJD6 were examined with CCK-8 assay while apoptosis was examined using flow cytometry. Meanwhile, migration and invasiveness were analyzed using transwell assays. Bindings between LINC00839 and miR-519d-3p, miR-519d-3p and JMJD6 were measured by luciferase reporter assays. LINC00839 was upregulated in LC cells and its knockdown resulted in reduced cell viability, migratory ability and invasion with increased cell apoptosis. MiR-519d-3p was the target gene of LINC00839 and its expression was reduced by LINC00839 overexpression. JMJD6 was directly targeted and suppressed at the level of mRNA and protein expression by miR-519d-3p. Moreover, miR-519d-3p overexpression resulted in low LC cell viability, migration, invasiveness but a high apoptosis rate. Furthermore, mRNA and protein expressions of JMJD6 were upregulated by LINC00839 overexpression. LINC00839 competitively sponged miR-519d-3p, increasing JMJD6 expression, LC cell viability, invasion, migratory abilities and decreasing apoptosis rates in A549 and H460 lung cancer cells, which were hindered after JMJD6 knockdown. LINC00839/miR-519d-3p/JMJD6 axis mediated cell viability, apoptosis, and migration and invasiveness of H460 lung cancer cells.