Apoptosis In Colon Cancer Cells Research Articles

SP1-induced circ_0017552 modulates colon cancer cell proliferation and apoptosis via up-regulation of NET1

Colon cancer (CC) is a common malignancy over the world and its morbidity and mortality significantly went up in China in recent years. Molecular functions in cancers have gradually been the pivot subject in cancer research. Neuroepithelial cell transforming 1 (NET1) was reported to contribute to prostate cancer and gastric cancer. Our study figured out that NET1 was overexpressed in CC cells. Then, loss-of-function assays revealed that NET1 facilitated CC cell proliferation and repressed CC cell apoptosis. Next, miR-338-3p was confirmed to target NET1. After that, we verified that circ_0017552 which originates from NET1 could positively modulate NET1 expression. Besides, circ_0017552 was a sponge of miR-338-3p. Rescue assays’ results demonstrated that circ_0017552 could regulate CC cell proliferation and apoptosis through up-regulation of NET1. A transcription factor named Sp1 (SP1) was found to be present in circ_0017552. SP1 induced transcription of circ_0017552 to facilitate CC cell proliferation and inhibit CC cell apoptosis. In a word, SP1-induced circ_0017552 regulated CC cell proliferation and apoptosis through miR-338-3p/NET1 axis.

Macromolecules with predominant β-pleated sheet proteins in extracellular vesicles released from Raphanus sativus L. var. caudatus Alef microgreens induce DNA damage-mediated apoptosis in HCT116 colon cancer cells

Plant-derived bioactive macromolecules (i.e., proteins, lipids, and nucleic acids) were prepared as extracellular vesicles (EVs). Plant-derived EVs are gaining pharmaceutical research interest because of their bioactive components and delivery properties. The spherical nanosized EVs derived from Raphanus sativus L. var. caudatus Alef microgreens previously showed antiproliferative activity in HCT116 colon cancer cells from macromolecular compositions (predominantly proteins). To understand the mechanism of action, the biological activity studies, i.e., antiproliferation, cellular biochemical changes, DNA conformational changes, DNA damage, apoptotic nuclear morphological changes, apoptosis induction, and apoptotic pathways, were determined by neutral red uptake assay, synchrotron radiation-based Fourier transform infrared microspectroscopy, circular dichroism spectroscopy, comet assay, 4′,6-diamidino-2-phenylindole (DAPI) staining, flow cytometry, and caspase activity assay, respectively. EVs inhibited HCT116 cell growth in concentration- and time-dependent manners, with a half-maximal inhibitory concentration of 675.4 ± 33.8 μg/ml at 48 h and a selectivity index of 1.5 ± 0.076. HCT116 treated with EVs mainly changed the cellular biochemical compositions in the nucleic acids and carbohydrates region. The DNA damage caused no changes in DNA conformation. The apoptotic nuclear morphological changes were associated with the increased apoptotic cell population. The apoptotic cell death was induced by both extrinsic and intrinsic pathways. EVs have potential as antiproliferative bioparticles.

Retraction: MiR-34b inhibits the proliferation and promotes apoptosis in colon cancer cells by targeting Wnt/β-catenin signaling pathway.

Retraction: MiR-34b inhibits the proliferation and promotes apoptosis in colon cancer cells by targeting Wnt/β-catenin signaling pathway.

Structure-Activity Relationship Study of Biselyngbyolide B Reveals Mitochondrial Fission-Induced Cytotoxicity in Cancer.

A systematic structure-activity relationship study of the potent anticancer marine macrolide biselyngbyolide B has been accomplished. A total of 11 structural variants of the parent natural product, of which 2 are natural analogues, have been studied against a human colorectal carcinoma cell line. The requisite functional units of the parent molecule responsible for the cytotoxic activities have been disclosed. Biselyngbyolide C, one of the natural analogues of biselyngbyolide B, has been studied in depth to explore its molecular mechanism. Interestingly, the in vitro data demonstrated an induction of dynamin-related protein 1-mediated mitochondrial fission and reactive oxygen species production which led to activation of ASK1/P38/JNK-mediated apoptosis in colon cancer cells as an important pathway for biselyngbyolide B-mediated cytotoxicity. Notably, this study revealed that a macrolide participated in mitochondrial fission to promote apoptosis of cancer cells, providing new insight.

The apoptotic effects of progesterone and testosterone on colon cancer (SW480) cells

Introduction: The association of sex steroids with cancer cell proliferation has been reported in recent studies; however, the findings are still controversial. The present study aimed to determine the cytotoxic effects of progesterone and testosterone on colon cancer (SW480) cells and to evaluate the expression levels of Bcl-2 and Bax genes in SW480 cells. Materials and Methods: The SW480 cell line was divided into a control group (untreated) and groups treated with 125, 250, 500, and 1000 μg/mL of testosterone and progesterone. Cell viability was quantified by the MTT assay. qRT-PCR was performed to evaluate gene expression levels. Flow cytometry was used to assess the apoptosis in cancer cells. Data were analyzed using the student's t-test and ANOVA. Results: The expression level of the Bax gene significantly decreased in SW480 cells exposed to a cytotoxic dose of progesterone. Moreover, the expression level of the Bax gene significantly increased in the SW480 cells exposed to a cytotoxic dose of testosterone. Conclusion: The results of the present study showed that testosterone might affect the apoptosis of colon cancer cells at low concentrations. Studies have shown that progesterone can induce tumor cell death in cancer cells. Accordingly, the clinical use of testosterone and progesterone therapy for cancer treatment is highly controversial.

Prevalence of Hypothyroidism and Hyperthyroidism in Women of Reproductive Ages in Kabul

Introduction: The association of sex steroids with cancer cell proliferation has been reported in recent studies; however, the findings are still controversial. The present study aimed to determine the cytotoxic effects of progesterone and testosterone on colon cancer (SW480) cells and to evaluate the expression levels of Bcl-2 and Bax genes in SW480 cells. Materials and Methods: The SW480 cell line was divided into a control group (untreated) and groups treated with 125, 250, 500, and 1000 μg/mL of testosterone and progesterone. Cell viability was quantified by the MTT assay. qRT-PCR was performed to evaluate gene expression levels. Flow cytometry was used to assess the apoptosis in cancer cells. Data were analyzed using the student's t-test and ANOVA. Results: The expression level of the Bax gene significantly decreased in SW480 cells exposed to a cytotoxic dose of progesterone. Moreover, the expression level of the Bax gene significantly increased in the SW480 cells exposed to a cytotoxic dose of testosterone. Conclusion: The results of the present study showed that testosterone might affect the apoptosis of colon cancer cells at low concentrations. Studies have shown that progesterone can induce tumor cell death in cancer cells. Accordingly, the clinical use of testosterone and progesterone therapy for cancer treatment is highly controversial.

Hsa_circ_0101050 accelerates the progression of Colon cancer by targeting the miR-140–3 p/MELK axis

BackgroundCircular RNAs (circRNAs) are involved in the progression of colon cancer (CC). This study aimed to examine the role of a new circRNA circ_0101050 in CC. MethodsDual-luciferase reporter and RNA immunoprecipitation analyses were performed to validate the target relationships among maternal embryonic leucine zipper kinase (MELK), microRNA (miR)-140–3 p, and circ_0101050. Expression levels were calculated using western blotting and/or quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Western blotting was performed to evaluate the relative expression of Bcl-2 and Bax proteins to determine cell death. Cell Counting Kit-8 (CCK-8) and colony formation assays were performed to determine the proliferative potential of CC cells. The migration rate of CC cells was evaluated using wound healing assays. Tumor formation tests were performed to determine the effect of circ_0101050 on tumor development in vivo. ResultsElevated levels of circ_0101050 and MELK were observed in CC. By inhibiting circ 0,101,050 or MELK, CC cell proliferation and migration were inhibited, but CC cell apoptosis was promoted. Silencing circ_0101050 also inhibited CC growth in vivo. We also found that miR-140–3 p was downregulated, which alleviated the repressive effects of circ_0101050 knockdown on proliferating and migrating CC cells, as well as the stimulating effect on apoptosis. In addition, the absence of MELK alleviated the effects of miR-140–3 p downregulation, which enhanced CC cell malignancy. ConclusionsCirc_0101050 exacerbates malignant phenotypes in CC by targeting the miR-140–3 p/MELK axis. These findings suggested that the circ_0101050/miR-140–3 p/MELK network may be a prospective target for CC treatment.

Remedy on Breast Cancer

The fundamental barrier to powerful remedy for breast maximum cancers is still multidrug resistance due to its severe natural outcomes. The triterpenoid molecule ursolic acid has been considered a capability neoplastic chemo preventive medicine. In numerous preclinical trials an aromatase inhibitor known as letrozole is used to treat Post-Menopausal Women with superior habitual and metastatic breast cancer. The authors may be able to discover a new remedy for the treatment of breast most cancers through identifying the ones who've element consequences much like those of letrozole the maximum aspect results were positioned to be shared through letrozole and the dopaminergic agonist ropinirole in line with research dopaminergic agonist’s purpose apoptosis in Leukaemia, Neuroblastoma, Colon, Ovarian and Breast Cancer Cells. Heart failure, esophageal cancer, lymphedema, bone loss are the side effects observed after treating breast cancer.

Abstract 507: HLS-22001 induces G2/M cell cycle arrest and apoptotic cell death via tubulin depolymerization in colon cancer

Abstract Colorectal cancer (CRC) is one of the main malignant tumors and among the leading cause of death in cancer patients worldwide considering that recurrence and chemotherapeutic drug resistance are highly common in the advanced stage of CRC. Mutations in KRAS and BRAF occur frequently in colorectal cancers, and abnormal cell cycles caused by these mutations affect tumor progression and metastasis. Accordingly, inhibition of cell cycle has been a potential target for colorectal cancers and therefore, we have developed a new lead compound, HLS-22001. Our studies confirmed that HLS-22001 inhibited the proliferation of several cancer cells and significantly induced G2/M arrest and apoptosis of colon cancer cells and chemotherapy resistant colon cancer cells. The docking model studies showed that HLS-22001 was expected to bind to the colchicine binding site of beta-tubulin, and in fact, as a tubulin inhibitor, it had the effect of inhibiting tubulin dimerization and polymerization in the microtubule dynamics. Consistently, in xenograft mouse model, oral administration of HLS-22001 significantly suppressed tumor weight and volume without acute toxicity in mice. Collectively, these results suggest further development of HLS-22001 as a novel and promising oral drug for colorectal cancer. Citation Format: Chi-hyun Ahn, Gyu-beom Jang, Chunhwa Kim, Junho Lee, Taewon Kim, Youngeun Yang, Eunji Cho, Minchae Kim, Yun-tai Kim, Yong-Hae Han, Heebum Kang. HLS-22001 induces G2/M cell cycle arrest and apoptotic cell death via tubulin depolymerization in colon cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 507.

Abstract 4377: AT rich interaction domain 5a promotes gastrointestinal tumorigenesis by regulating YAP and STAT3 pathways

Abstract Background: Chronic inflammation and an inflammatory cytokine, interleukin(IL)-6, play important roles in gastrointestinal tumorigenesis and metastasis. Recently, autocrine IL-6 has been reported to promote cancer development and progression in gastrointestinal cancer. However, it is still unknown how IL-6 level is regulated in gastrointestinal cancer cells. RNA-binding proteins (RBPs) are known to be one of the regulatory mechanisms of cytokine production, including IL-6, especially in immune cells. AT rich interaction domain 5a (Arid5a), one of the RBPs, has been reported to bind to IL6 3’UTR and regulates its stability and expression. Therefore, we aimed to elucidate the role of Arid5a in gastrointestinal cancer, especially gastric and colon cancer. Methods: Human gastric and colon cancer cell lines were used in this study. Arid5a knocked-down gastric and colon cancer cells were generated with lentiviral transduction of shRNAs targeting Arid5a and their phenotypes were investigated by several assays including MTT, apoptosis and sphere formation assays. Bulk RNA-seq analysis was performed using Arid5a knocked-down gastric and colon cancer cells. Results: In both human gastric and colon cancer cell lines, Arid5a knockdown suppressed cancer cell proliferation and spheroid formation, and increased apoptosis. Unexpectedly, IL6 mRNA expression was not correlated with Arid5a expression level. We found that Arid5a knockdown suppresses the activation of YAP and STAT3 by western blot analysis. We identified several new Arid5a target genes by bulk RNA-seq analysis. Conclusion: Arid5a plays an important role in the regulation of cancer cell proliferation, apoptosis and stemness in human gastric and colon cancer cells, perhaps independently of IL-6. Arid5a regulates YAP and STAT3 pathways by unknown mechanisms. We are now investigating how Arid5a regulates YAP and STAT3 pathways by focusing new Arid5a target genes. Citation Format: Koji Taniguchi, Kazuya Hamada, Shugo Tanaka, Hiroyuki Kurosu, Issei Kawakita, Kentaro Kumagai, Kentaro Nakazono, Sari Iwasaki, Satoshi Tanaka. AT rich interaction domain 5a promotes gastrointestinal tumorigenesis by regulating YAP and STAT3 pathways [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4377.

Effects of Viable and Heat-Inactivated Bifidobacterium longum D42 on Proliferation and Apoptosis of HT-29 Human Colon Cancer Cells.

Bifidobacterium longum is a common probiotic; both viable and heat-inactivated Bifidobacterium longum have many probiotic effects, such as anticancer effects. But some mechanisms of anticancer effects are still unclear, especially for heat-inactivated probiotics. In this study, we analyzed the effects of viable and heat-inactivated Bifidobacterium longum D42 on human colon cancer cells (HT-29). Cell proliferation, membrane permeability and apoptosis were detected by using the CCK-8 method, LDH method and Annexin V-FITC/PI kits. The ROS level and mitochondrial membrane potential were examined using the fluorescent probes DCFH-DA and JC-1. Real-time fluorescence quantitative PCR (RT-qPCR) and Western blot were used to detect the expression of mitochondrial apoptosis pathway genes and proteins. The results showed that viable and heat-inactivated Bifidobacterium longum D42 at concentrations of 1 × 106 CFU/mL significantly inhibited the proliferation of and increased the level of LDH release of HT-29 colon cancer cells. We found that they could increase the apoptosis rate of HT-29 cells. Moreover, they could also induce apoptosis by inducing cells to produce ROS and destroying the mitochondrial membrane potential of cells. Further studies found that they could increase the mRNA transcription and protein expression levels of the Caspase-3, Caspase-9 and Bax genes in cells, and reduce the mRNA transcription and protein expression levels of the Bcl-2 gene. In summary, our findings revealed that viable and heat-inactivated Bifidobacterium longum D42 have inhibitory effects on proliferation and promote the apoptosis of human colon cancer cells, and also have certain adjuvant drug therapeutic effects and have potential application value in the adjuvant treatment of colon cancer.

Curcumin targeting miR-761 influences proliferation and apoptosis of colon cancer cells through GSK-3β regulation

Abnormal miR-761 expression involves in colon cancer and curcumin has a significant anti-tumor cell proliferation effect. In this study, we investigated whether curcumin targeting miR-761 can affect colon cancer cells. Control group (NC group), miR-761 Mimics group, and miR-761 Mimics+curcumin group were set up. miR-761 and GSK-3β levels were detected by RT-qPCR. Dual fluorescein report detected the relation between miR-761 and GSK-3β along with analysis of cell proliferation by cloning assay and apoptosis by flow cytometry. Compared with normal tissues, miR-761 expression in colon cancer tissues was lower (P <0.01), while GSK-3β level was higher (P < 0.01). Dual fluorescein report analysis showed GSK-3β as a target of miR-761. Compared with NC group, clone number in miR-761 Mimics group decreased, the proliferation capacity decreased, and apoptotic number increased. While compared with miR-761 Mimics group, clone number in miR-761 Mimics+curcumin cells increased, proliferation capacity increased, and apoptotic number decreased. Curcumin targeting miR-761 can inhibit GSK-3β expression, inhibit colon cancer cells proliferation and promote apoptosis. However, when the pCDNA-GSK-3β plasmid overexpresses GSK-3β, it can prevent the action of miR-761.

MT1G Regulates c-MYC/P53 Signal to Inhibit Proliferation, Invasion and Migration and Promote Apoptosis in Colon Cancer Cells.

Colon cancer is a common and malignant cancer featuring high morbidity and poor prognosis. This study was performed to explore the regulatory role of MT1G in colon cancer as well as its unconcealed molecular mechanism. The expressions of MT1G, c-MYC, and p53 were assessed with the application of RT-qPCR and western blot. The impacts of MT1G overexpression on the proliferative ability of HCT116 and LoVo cells were measured by CCK-8 and BrdU incorporation assays. Additionally, transwell wound healing, and flow cytometry assays were employed to evaluate the invasive and migrative capacities as well as the apoptosis level of HCT116 and LoVo cells. Moreover, the activity of the P53 promoter region was assessed with the help of a luciferase reporter assay. It was found that the expressions of MT1G at both mRNA and protein levels were greatly decreased in human colon cancer cell lines, particularly in HCT116 and LoVo cell lines. After transfection, it was discovered that the MT1G overexpression suppressed the proliferation, migration and invasion but promoted the apoptosis of HCT116 and LoVo cells, which were then partially reversed after overexpressing c-MYC. Additionally, MT1G overexpression reduced c-MYC expression but enhanced the p53 expression, revealing that the MT1G overexpression could regulate c-MYC/P53 signal. Elsewhere, it was also shown that c-MYC overexpression suppressed the regulatory effects of MT1G on P53. To conclude, MT1G was verified to regulate c-MYC/P53 signal to repress the proliferation, migration and invasion but promote the apoptosis of colon cancer cells, which might offer a novel targeted-therapy for the improvement of colon cancer.

Synthesis of 1-(4-chlorobenzoyl)-4-(dimethylamino) pyridin-1-ium chloride and determination of cytotoxicity and apoptosis in human colon cancer cells

BackgroundIn this experiment, we synthesized a new compound, 1-(4-chlorobenzoyl)-4-(dimethylamino) pyridin-1-ium chloride (SM-9), and examined its toxicity and anticancer activity in human colon cancer (HCT-116) cells. MethodsWe uncovered the underlying mechanisms of cell toxicity and apoptosis due to SM-9 compound exposure in HCT-116 cells by using the MTT assay and protein profiling array and measuring gene expression levels using reverse transcription-polymerase chain reaction. ResultsOur data show that the SM-9 compound activated the caspase-3, caspase-8, p21, p27, and p53 proteins involved in the apoptosis of HCT-116 cells, thereby inducing cytotoxicity, the formation of reactive oxygen species, and apoptosis. The results of this study show that the SM-9 compound has advantageous qualities and must be taken as an anticancer medication. We conclude that the SM-9 compound exerted an anticancer effect by inducing the apoptotic pathways in human colon cancer (HCT-116) cells.

Therapeutic effects of coptisine derivative EHLJ7 on colorectal cancer by inhibiting PI3K/AKT pathway

Colorectal cancer (CRC) is the third most common cancer in the world with high mortality rate. EHLJ7 is a quaternary coptisine derivative synthesized by our institute. In this study, the role and mechanism of EHLJ7 on CRC are further elucidated. Using target fishing, colon cancer-associated target screening and molecular docking analysis, PI3K/AKT pathway was selected for the target of EHLJ7 at CRC. Results of Flow cytometry, wound healing assay and transwell migration assay confirmed that EHLJ7 could inhibit migration and apoptosis of colon cancer cells by specifically inhibiting PI3K/AKT pathway in vitro. Xenograft tumor models and a newly established azoxymethane (AOM)/dextran sulfate sodium (DSS)/Peptostreptococcus anaerobiu (P.anaerobius)-induced CRC mouse model are applied to access the anti-cancer action and mechanism of EHLJ7 using western-blot, immunohistochemistry and analysis of exosomes. The key findings in this study are listed as follows: (1) EHLJ7 exerts superior anti-tumor effect with good safety on Xenograft tumor model and CRC model; (2) EHLJ7 exerted its anti-CRC effect by specifically inhibiting PI3K/AKT pathway and apoptosis in vivo and in vitro. In summary, we demonstrated that EHLJ7 exerts therapeutic effect against CRC by PI3K/AKT pathway, which made it possible as a potentially effective compound for the treatment of CRC.

ZMIZ1 Regulates Proliferation, Autophagy and Apoptosis of Colon Cancer Cells by Mediating Ubiquitin-Proteasome Degradation of SIRT1.

There are nearly 1.15 million new cases of colon cancer, as well as 586,858 deaths from colon cancer worldwide in 2020. The aim of this study is to reveal whether ZMIZ1 can control the fate of colon cancer cells and the mechanism by which it functions. Specific shRNA transfection was used to knock down the expression of ZMIZ1 in colon cancer cell lines (HCT116 and HT29), and cell proliferation was detected using EdU and CCK-8 reagents, apoptosis by flow cytometry, and autophagy by western blot. The interaction of ZMIZ1 and SIRT1 was analyzed. Knockdown of ZMIZ1 significantly inhibited autophagy and proliferation, and induced apoptosis of HCT116 and HT29 cells. The mRNA level of SIRT1 was not affected by ZMIZ1 knockdown, but the protein level of SIRT1 was significantly decreased and the protein level of the SIRT1-specific substrate, acetylated FOXO3a, was reduced. Immunoprecipitation assays identified the interaction between SIRT1 and ZMIZ1 in HCT116 and HT29 cells. ZMIZ1 increased intracellular ubiquitination of SIRT1. Knockdown or pharmacological inhibition of SIRT1 neutralized the effects of ZMIZ knockdown on proliferation, autophagy and apoptosis in HCT116 and HT29 cells. ZMIZ1 may control the fate of colon cancer cells through the SIRT1/FOXO3a axis. Targeting ZMIZ1 would be beneficial for the treatment of colon cancer.

Organic Extract of Streptomyces Induces Apoptosis, Anti-Proliferation and Cell-Cycle Arrest in Colon Cancer Cells: Caco-2 and HCT116 Cell Line as Surrogate Model

Background: Colorectal cancer (CRC) is a prevalent and very lethal malignancy, resulting in more than one million deaths and nearly two million newly diagnosed cases in the year 2018. Streptomyces bacteria are a potential source of conventional compounds, as their extract contains bioactive chemicals with antiproliferative effects in cell culture settings. The aim of this research was to investigate the antiproliferative effects of the Streptomyces ethyl acetate fraction against the Caco-2 and HCT116 cell line in addition to its fundamental mechanisms. Methods: We examined the effects of Streptomyces extract on colon cancer cell lines Caco-2 and HT-116 by incubating the cells with and without the extract. Antiproliferative effects are analyzed using the MTT cell proliferation assay, cell cycle analysis and flow cytometric detection of Annexin V/PI apoptosis. The formation of intracellular ROS was measured, in addition to Western Blot for Bax, Bcl2 and caspase-3 activation. Result: Our findings showed the dose-dependent inhibition of cell growth by streptomyces extract. Both Caco-2 and HT-116 cells treated with streptomyces extract displayed the beginning of apoptotic events and G1 cell-cycle arrest. Additionally, treat with the streptomyces extract significantly increased (P less than 0.05) ROS production, Bax and cleaved-caspase-3 were increased, while Bcl-2 was downregulated, as determined by western blotting.

MiR-373 promotes invasion and metastasis of colorectal cancer cells via activating ERK/MAPK pathway

To explore the relationship between miR-373 and the occurrence and development of colorectal cancer. Additionally, it aims to predict the potential cellular signaling pathways and regulatory mechanisms in which miR-373 may be involved and provides a theoretical basis and experimental evidence for the clinical application of miR-373 as a potential biomarker, molecular target, and prognostic indicator in colorectal cancer. Real-time quantitative PCR is used to analyze the expression of miR-373 in human colorectal cancer cell lines and normal human colonic epithelial cells. Further validation of the differential expression of miR-373 in colorectal cancer cell lines is being performed. Biological functions such as cell proliferation, invasion and apoptosis are being detected by MTT, CCK-8, transwell, cell cycle analysis, and flow cytometry experiments to verify the changes in the biological behavior of colon cancer cells after overexpression and interference of miR-373 in SW-480 cells and to explore the effects of miR-373 on cell proliferation, invasion, and apoptosis in colon cancer cells. Proteomic analysis is being conducted on proteins extracted from miR-373 overexpressing SW480 cells, and mass spectrometry is used for protein identification. GO, KEGG, and enrichment analysis are being employed to analyze the significantly differentially expressed proteins. The expression levels of pathway-related proteins are being verified using Western blot. Overexpression of miR-373 increased the invasive and metastatic ability of SW-480 cells; knockdown of miR-373 decreased the invasive and metastatic ability of SW-480 cells. However, there was no statistically significant effect on cell proliferation and apoptosis in SW-480 cells. Proteomic analysis identified 78 differentially expressed proteins based on fold change (FC) > 1.2 and P < 0.05. Annotation of differentially changed proteins revealed that the MAPK signaling pathway, PI3K-Akt signaling pathway, and FAK signaling pathway may play crucial roles in the migration and invasion of colorectal cancer. Western blot analysis showed that overexpression of miR-373 significantly increased the levels of p-ERK1/2 in SW480 cells. miR-373 may activate the ERK/MAPK signaling pathway to promote the invasion and migration of colorectal cancer cells.

Vitex negundo L. leaf extract suppresses the cell cycle and promotes apoptosis in colon cancer cells

Vitex negundo L. leaf extract suppresses the cell cycle and promotes apoptosis in colon cancer cells

Metformin Suppresses the Proliferation and Promotes the Apoptosis of Colon Cancer Cells Through Inhibiting the Expression of Long Noncoding RNA-UCA1 [Retraction

[This retracts the article DOI: 10.2147/OTT.S245091.].