Apoptosis In HCT116 Cells Research Articles

Artemetin Inhibits Cell Growth and Activates Caspase-dependent Apoptotic Cell Death Colon Cancer HCT-116 Cells

Background Colon cancer, a prevalent form of gastrointestinal malignancy, poses a significant public health issue globally. The onset of colon cancer is a complex mechanism implicating genetic and environmental factors, including dietary habits and lifestyle choices. Purpose The current study was undertaken to investigate the anti-tumor effects of artemetin against colon cancer cells. Materials and Methods The influence of artemetin on the proliferation of HCT-116 cells was evaluated with an MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) test. Also, the extent of apoptosis in both untreated and artemetin-exposed HCT-116 cells was studied using a dual staining technique. The activities of the caspase enzymes (caspase-3, -8, and -9) in both untreated and artemetin-exposed HCT-116 cells were evaluated using a commercial diagnostic kit. Results The administration of several dosages of artemetin significantly suppressed the HCT-116 cells dose-dependently. Furthermore, artemetin treatment significantly induced apoptosis in HCT-116 cells, which is evidenced by dual staining assay. Artemetin treatment also elevated the caspase-3, -8, and -9 activities in the colon cancer cells. Conclusion The present study revealed that artemetin possesses anti-cancer activities against colon cancer, reducing cell viability and inducing caspase-mediated apoptosis in HCT-116 cells. Consequently, the present findings indicate artemetin as a favorable anti-tumor candidate for future colon cancer therapy.

The role of HM13 expression and its relationship to PI3K/Akt and p53 signaling pathways in colorectal cancer.

The role of HM13 expression and its relationship to PI3K/Akt and p53 signaling pathways in colorectal cancer.

PepGAT, a chitinase-derived peptide, alters the proteomic profile of colorectal cancer cells and perturbs pathways involved in cancer survival.

PepGAT, a chitinase-derived peptide, alters the proteomic profile of colorectal cancer cells and perturbs pathways involved in cancer survival.

Preparation, characterization, and induced human colon cancer HCT-116 and HT-29 cell apoptosis performance of selenium nanoparticles stabilized by longan polysaccharides.

Preparation, characterization, and induced human colon cancer HCT-116 and HT-29 cell apoptosis performance of selenium nanoparticles stabilized by longan polysaccharides.

Structural characterization of a polysaccharide from Qi-Gui herb pair and its anti-tumor activity in colon cancer cells.

Astragalus membranaceus (Fisch.) Bunge and Angelica sinensis (Oliv.) Diels forms a classic herb pair (Qi-Gui her pair) in Chinese medicine, which was commonly used for treating menstrual anemia and microvascular ischemic diseases. While polysaccharides are known to be key bioactive components of the Qi-Gui herb pair, their structural characteristics and pharmacological activities remain underexplored. In this research, a homogeneous polysaccharide with a molecular weight of 18.1kDa was isolated, and its structure was analyzed via high pressure size exclusion chromatography, high performance liquid chromatography, gas chromatography mass spectrometry, and nuclear magnetic resonance spectroscopy. The structural analysis revealed that AAPS-1a was composed of α-T-Glcp (5.9%), β-1,3-Galp (3.9%), α-1,4-Manp (3.6%), α-1,4-Galp (2.1%), α-1,4-Glcp (2.8%), and α-1,6-Glcp (81.7%). Furthermore, NMR analysis revealed that AAPS-1a consists of a repeat unit: α-T-Glcp-(1→4)-α-Galp-(1→4)-α-Manp-(1→4)-α-Glcp-(1→[6)-α-Glcp-(1]n→3)-β-Galp-(1→. In vitro studies showed that AAPS-1a could significantly inhibit the proliferation of HCT116 cells, and induces G1 arrest and G2/M arrest, as well as apoptosis of HCT116 cells. This study presents the inaugural report establishing a connection between the structural characteristics of Qi-Gui herbal polysaccharides and their anti-colon cancer activity, demonstrating that AAPS-1a holds promise as a therapeutic agent for the treatment of colon cancer.

Acetylated Dendrobium huoshanense polysaccharide: a novel inducer of apoptosis in colon cancer cells via Fas-FasL pathway activation and metabolic reprogramming.

Not all polysaccharides function as antitumor drugs, nor do they universally possess the same advantages regarding safety and biocompatibility. Those polysaccharides that are effective antitumor agents typically demonstrate superior safety profiles and biocompatibility compared to synthetic anticancer drugs, which can exhibit high toxicity and harmful side effects. Dendrobium huoshanense polysaccharide (DHP) has been recognized for its potential bioactive properties, particularly in anti-tumor treatment. This study investigates the effects of DHP on the proliferation and apoptosis of HCT116 colon cancer cells. DHP was extracted according to previously published experimental methods. The inhibitory effects of DHP were evaluated using IEC6, Caco-2, and HCT116 cell lines, with changes in cell morphology observed via transmission electron microscopy. After establishing the conditions for DHP administration, flow cytometry was employed to assess its effects on apoptosis, reactive oxygen species (ROS), and mitochondrial membrane potential of HCT116 cells. Additionally, immunoprecipitation, quantitative real-time polymerase chain reaction (qRT-PCR), Western blotting, and biomarker detection were utilized to investigate the mechanisms underlying DHP's inhibition of HCT116 cells and its impact on metabolic reprogramming. In the present study, we observed that DHP treatment at 600 μg/ml for 24 h reduced HCT116 cell viability to 54.87%. In contrast, the inhibitory effect of DHP on the viability of IEC6 and Caco-2 cells was relatively mild. The specific mechanism involves DHP activating the mitochondrial apoptotic pathway leading to the downregulation of key metabolic intermediates and enzymes such as uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) and ST6Gal-I. By inhibiting ST6Gal-I activity, DHP activates the Fas/FasL signaling pathway. Additionally, DHP-induced ROS production effectively triggers apoptosis in HCT116 cells. Our study demonstrates that DHP effectively inhibits the proliferation and induces apoptosis in HCT116 colon cancer cells through the activation of the Fas-FasL signaling pathway and metabolic reprogramming. The selective inhibitory effect of DHP on HCT116 cells, the activation of both death receptor and mitochondrial apoptotic pathways, and the modulation of metabolic reprogramming provide novel insights into the potential therapeutic strategies for colon cancer.

New indolin-2-ones, possessing sunitinib scaffold as HDAC inhibitors and anti-cancer agents with potential VEGFR inhibition activity; design, synthesis and biological evaluation.

New indolin-2-ones, possessing sunitinib scaffold as HDAC inhibitors and anti-cancer agents with potential VEGFR inhibition activity; design, synthesis and biological evaluation.

Folate receptor-targeted and pH-tunable dextran modified geraniol-protein nano-scaffolds stir up oxidative assault and apoptotic killing of HCT-116 colorectal cancer cells

Folate receptor-targeted and pH-tunable dextran modified geraniol-protein nano-scaffolds stir up oxidative assault and apoptotic killing of HCT-116 colorectal cancer cells

Licorice Extract Isoliquiritigenin Increased Cytosol Calcium and Induced Apoptosis in Colon Cancer Cells via Transient Receptor Potential Vanilloid-1.

Colorectal cancer (CRC) is the third most common malignant tumor, and the fifth cause of cancer-related death in China, while chemotherapy is the primary strategy for CRC. Transient receptor potential (TRP) channels are non-selective cation channels while modulating the expression or activity of TRP channels results in the regulation of Ca2+ influx. Previous studies have shown that TRP members with altered expression or channel activity are presented in CRC cells, which made them become promising therapeutic targets. Isoliquiritigenin (ISL), one of the major bioactive ingredients from traditional Chinese medicine licorice, was reported to exhibit anti-cancer properties such as induce apoptosis in CRC cells, but the underlying mechanism was not fully understood, whether its anticancer activity was related to regulating intracellular calcium and TRP channels remains for further investigation. The study aims to investigate the effect of ISL on altering cytosol calcium in CRC cells and elucidate its potential molecular mechanism. The study was conducted on 2 CRC cell lines HT29 and HCT116. Changes of cytosol calcium was indicated by live cell Ca2+ imaging. Expression level of TRPV1 was determined by western blot. Cell apoptosis was detected by flow cytometry with Annexin V-FITC/PI staining. ISL significantly increased cytosol calcium in HT29 and HCT116 cells. The ISL-induced increasing calcium ions were from both calcium influx and intracellular calcium release. ISL co-culture directly upregulated the expression of transient receptor potential vanilloid-1 (TRPV1) in colon cancer cells. Inhibition of TRPV1 by capsazepine (CapZ) abrogated the ISL-induced calcium influx and ISL-induced apoptosis in HT29 and HCT116 cells. This study illustrates, for the first time, that ISL increased cytosol calcium concentration and induced apoptosis via TRPV1 in colon cancer cells, giving a new understanding of the underlying mechanism of its anti-cancer ability and making it a potential regulator for TRPV1.

Lactobacillus plantarum SMUM211204 Exopolysaccharides Have Tumor-Suppressive Effects on Colorectal Cancer by Regulating Autophagy via the mTOR Pathway.

Probiotics have demonstrated their ability to suppress tumors in cell lines and mouse models. However, the precise molecules responsible for these effects remain unidentified. We focused on isolating and analyzing the exopolysaccharides (EPSs) produced by Lactobacillus plantarum (L. plantarum) SMUM211204. Our findings confirm that EPSs impair the growth of HCT116 cells and induce autophagy and apoptosis. Moreover, further experimental evidence demonstrates that EPSs diminish the expression of phosphorylation levels of PI3K, AKT, and mTOR. In contrast, they boost the expression of AMPKa, elevate the ULK1 level, and increase the protein LC3-II/I ratio. Furthermore, when rapamycin is employed to impede EPS-induced autophagy, it results in an enhancement of apoptosis and cell death in HCT116 cells. To validate these findings in vivo, we conducted an animal study using a colorectal cancer xenograft model. The results showed a significant reduction in tumor volume and weight in the EPS-treated group compared with the control group. Immunohistochemical analysis of tumors indicated increased expressions of LC3 and caspase-3, along with decreased levels of phospho-PI3Kinase, phospho-AKT, and P62, consistent with in vitro findings. Our study proved that EPSs have an inhibitory effect on colorectal cancer and can be used as a preventive and therapeutic drug for cancer.

Discovery of Novel Oxazolo[4,3-f]purine Derivatives as Antitumor Agents through PPIA Interaction.

54 novel oxazolo [4,3-f]purine derivatives were designed, synthesized, and evaluated for antitumor activity, among which compound 20b exhibited potent activity against several cancer cell lines. Compound 20b inhibited cell metastasis, arrested the cell cycle in the G0/G1 phase, and induced apoptosis in HCT116 cells. Mechanistic studies revealed that 20b increased ROS levels and led to DNA damage, endoplasmic reticulum (ER) stress, and mitochondrial dysfunction in HCT116 cells. Limited proteolysis-small molecule mapping (LiP-SMap), drug affinity responsive target stability (DARTS) assay, cellular thermal shift assay (CETSA), and surface plasmon resonance (SPR) experiments provided evidence that compound 20b bound to PPIA with a KD value of 0.52 μM. siRNA assay indicated that 20b-mediated antiproliferative and antimigration activities were abolished and that the PPIA/MAPK signaling pathway was inhibited when PPIA was silenced in HCT116 cells. Significantly, compound 20b presented significant anticolorectal cancer efficacy in vivo without obvious toxicity. These results indicate that 20b may serve as a novel anticancer agent targeting PPIA, meriting further attention in antitumor drug research.

Enhancement of apoptosis in HCT116 and HepG2 cells by Coix lacryma-jobi var. lacryma-jobi seed extract in combination with sorafenib

Enhancement of apoptosis in HCT116 and HepG2 cells by Coix lacryma-jobi var. lacryma-jobi seed extract in combination with sorafenib

KW2478 and Cisplatin Synergistically Anti-colorectal Cancer by Targeting PI3K/AKT/mTOR Pathway.

The objective of this study is to examine the impact of KW-2478 combined with DDP on colorectal cancer cells both in vitro and in vivo and to elucidate the molecular mechanism of KW-2478 in colorectal cancer. qRT-PCR and Western blot were employed to assess HSP90 mRNA and protein expression in normal intestinal epithelial and colorectal cancer cells. DLD-1 and HCT116 were selected for the experiment. CCK-8 was used to detect cytotoxicity; apoptosis rate was measured using flow cytometry; Western blot was employed to measure the expression levels of apoptotic and PI3K/AKT/mTOR pathway proteins. HCT116 was used to construct a subcutaneous tumor model in nude mice. After treatment with KW-2478 and DDP, the growth rate, volume, and weight of the tumor were observed. The expression of Ki67 was detected by immunohistochemistry. Apoptosis of tumor cells was detected using TUNEL. Western blot was employed to measure the expression levels of apoptotic and PI3K/AKT/mTOR pathway proteins. HSP90 mRNA and protein levels were elevated in colorectal cancer cells compared to normal colorectal epithelial cells. HSP90 mRNA and protein expression levels were also significantly elevated in HCT116 and DLD-1 cells compared to other colorectal cancer cells. In DLD-1 and HCT116 cells, KW2478 and DDP inhibited cell viability. The combination of KW2478 and DDP exhibited a significantly higher inhibitory effect compared to either KW2478 or DDP alone. DDP markedly triggered apoptosis in HCT116 and DLD-1. KW2478 at 3 μg/ml and 6 μg/ml induced apoptosis in HCT116 cells but not in DLD-1 cells. The combination of KW2478 and DDP induced a significantly higher apoptosis rate as compared to either KW2478 or DDP alone. Treatment of HCT116 and DLD-1 with KW2478 or DDP alone increased Bax, Caspase9, and Caspase3 protein expression, while decreasing BCL-2. The KW2478+DDP combined treatment group exhibited more significant changes. Phosphorylation of PI3k, AKT, and mTOR decreased in the KW2478 or DDP treatment groups, with more significant changes observed in the KW2478 + DDP combination group. The growth rate, volume, and weight of subcutaneous tumors in the KW2478 or DDP treatment groups were significantly lower than control, and the KW2478+DDP combination group was more affected. Ki67 expression in subcutaneous tumors was reduced in the KW2478 or DDP treatment groups compared to the vehicle control group, with the lowest expression observed in the KW2478 + DDP combination group. The fluorescence intensity of subcutaneous tumors was higher in both the KW2478 and DDP treatment groups compared to the vehicle control group, and the KW2478 + DDP combination group exhibited the strongest fluorescence intensity among them. The combination of KW2478 and cisplatin inhibits colorectal cancer cell proliferation and induces apoptosis by regulating the PI3K/AKT/mTOR pathway.

Mcl-1 is a Gatekeeper Molecule to Regulate the Crosstalk Between Ferroptotic Agent-Induced ER Stress and TRAIL-Induced Apoptosis.

We previously reported that ferroptosis interplays with apoptosis through the integration of two independent pathways: the endoplasmic reticulum (ER) stress signaling pathway and the mitochondria-dependent apoptotic signaling pathway. In this study, we investigated a potential gatekeeper molecule, Mcl-1, between the two signal transduction pathways. Morphology studies and cell death analyses confirmed that a combination treatment of ferroptotic agent erastin (ERA) and apoptotic agent TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) synergistically enhances TRAIL-induced apoptosis in human pancreatic adenocarcinoma BxPC3 and human colorectal carcinoma HCT116 cells. We further observed that ERA upregulated the proapoptotic proteins PUMA (p53 upregulated modulator of apoptosis) and NOXA, as well as the anti-apoptotic protein Mcl-1 (myeloid cell leukemia sequence 1). These results suggest that ERA upregulates these molecules which results in maintenance of the balance between them. Interestingly, this balance was offset when BxPC3 cells and HCT116 cells were treated with ERA in combination with TRAIL. Our studies suggest that the imbalance between PUMA and NOXA and Mcl-1 during the combined treatment is responsible for ERA-enhanced TRAIL-induced apoptosis. This hypothesis was tested by employing a HCT116 Mcl-1 knock-in of phosphorylation site mutant (S121A/E125A/S159A/T163A) and investigated the synergistic interaction between the ERA and TRAIL. Along with morphology and cell death studies, immunoblotting analyses revealed that HCT116 Mcl-1 knock-in mutant cells effectively inhibited reduction of Mcl-1 and apoptosis promoted by the combination treatment. Moreover, ERA enhanced Mcl-1 inhibitor-induced apoptosis. Collectively, our studies suggest that Mcl-1 is a gatekeeper molecule between the ER stress pathway and the mitochondria-dependent apoptotic pathway.

Overexpression of lncRNA LINC00294 Induces Cell Cycle Arrest and Apoptosis in Colorectal Cancer by Regulating the miR‐499a‐5p/LARP4B Axis

ABSTRACTIncreasing long noncoding RNAs (lncRNAs) have been found to participate in regulating the progression of colorectal cancer (CRC), which is a common gastrointestinal malignancy. Here, the specific role and mechanisms of lncRNA LINC00294 were investigated in CRC. The expression levels of LINC00294, miR‐499a‐5p, and La‐related protein 4B (LARP4B) in CRC cells (HCT116 and SW620) and tissues were assessed by RT‐qPCR. The viability, proliferation, cell cycle, and apoptosis of HCT116 and SW620 cells were determined by CCK‐8, EdU, and flow cytometry assays. Protein levels of cell cycle and cell apoptosis markers were measured by western blot analysis. FISH assay was performed to evaluate the subcellular localization of LINC00294 in CRC cells. Luciferase reporter assay, RNA pull‐down assay, as well as RIP assay verified the interactions between miR‐499a‐5p and LINC00294 (or LARP4B). The xenograft model was established in mice to investigate the function of LINC00294 in vivo. LINC00294 presented a decreased expression level in CRC cells and tissues. LINC00294 overexpression suppressed the cell proliferative capacity, promoted cell cycle arrest, and induced cell apoptosis in CRC HCT116 and SW620 cells. LINC00294 interacted with miR‐499a‐5p, and miR‐499a‐5p targeted LARP4B. MiR‐499a‐5p was upregulated while LARP4B was downregulated in CRC cells. In rescue assays, LARP4B knockdown reversed the inhibition of LINC00294 overexpression on malignant phenotypes of HCT116 and SW620 cells. In the xenograft model, LINC00294 overexpression inhibited tumor growth in vivo. LINC00294 exerted an antitumor function in CRC by forming a LINC00294/miR‐499a‐5p/LARP4B regulatory network.

Chalcone Derivative 15 Induces Apoptosis in Human HOS, HCT116, and MCF-7 Cancer Cells

Chalcone Derivative 15 Induces Apoptosis in Human HOS, HCT116, and MCF-7 Cancer Cells

Green hydrothermal synthesis of gallic acid carbon dots: characterization and cytotoxic effects on colorectal cancer cell line

Colorectal cancer (CRC) remains a leading cause of cancer-related deaths worldwide, necessitating the development of novel therapeutic approaches. Carbon dots (CDs) have emerged as promising nanoparticles for biomedical applications due to their unique properties. Gallic acid (GA), an anticancer agent, is effective against various tumor types. This study explores the potential of gallic acid-derived carbon dots (GA-CDs) as an innovative anticancer agent against HCT-116 CRC cells, focusing on apoptosis signaling pathways. GA-CDs were synthesized using a one-pot hydrothermal method. Characterization was conducted using transmission electron microscopy (TEM), Fourier transform infrared (FT-IR) spectroscopy, and ultraviolet-visible (UV-vis) absorption spectroscopy. The cytotoxicity of GA and GA-CDs on HCT-116 cells was evaluated using the MTT assay at various concentrations over 24 and 48 h. Cellular uptake was assessed via fluorescence microscopy, and apoptosis was analyzed using acridine orange/propidium iodide (AO/PI) staining. Total RNA extraction followed by complementary DNA (cDNA) synthesis via reverse transcription-PCR was performed, and real time-PCR (Q-PCR) was conducted to examine the expression of apoptosis-related genes includingCaspase-3,Bax, andBcl-2. Characterization confirmed the successful synthesis of spherical GA-CDs. GA-CDs exhibited dose- and time-dependent cytotoxicity, with IC50 values of 88.55 μg ml-1for GA-CDs and 192.2 μg ml-1for GA after 24 h. Fluorescence microscopy confirmed the efficient uptake of GA-CDs by HCT-116 cells. AO/PI staining showed a significant increase in apoptotic cell numbers after treatment with GA-CDs. Q-PCR analysis revealed overexpression ofCaspase-3 andBaxgenes in GA-CD-treated cells, though no significant changes were observed in the expression ofBcl-2 or theBax/Bcl-2 ratio. GA-CDs demonstrated potent anticancer properties by inducing apoptosis and reducing cell viability in HCT-116 cells. These findings suggest the potential of GA-CDs as a novel therapeutic agent for CRC treatment, warranting further investigation into their mechanism of action andin vivoefficacy.

ONC206, an imipridone derivative, demonstrates anti-colorectal cancer activity against stem/progenitor cells in 3D cell cultures and in patient-derived organoids.

ONC206, an imipridone derivative, demonstrates anti-colorectal cancer activity against stem/progenitor cells in 3D cell cultures and in patient-derived organoids.

Biglycan promotes tumour proliferation and invasion in human colon cancers.

To investigate the role of biglycan (BGN) in colon cancer progression. The association between BGN mRNA levels and the survival time of patients with colon cancer was analysed by referencing data from the Gene Expression Omnibus and The Cancer Genome Atlas (TCGA). Gene Set Enrichment Analysis (GSEA) was conducted to explore gene sets and pathways associated with BGN. In vitro analyses were undertaken in HCT116 cells to analyse cell proliferation, migration, invasion, cell cycle control and apoptosis. GSEA, Western blot analysis and small interfering RNAs were used to explore the molecular mechanisms of BGN in colon cancer cells. Analysis of the pairs of tissues from colon cancer patients showed that BGN protein levels were higher in colon cancer tissues compared with adjacent non-tumour tissues. High BGN levels were significantly associated with shorter survival times. BGN knockdown inhibited cell proliferation, migration and invasion; and induced cell cycle arrest in the G0/G1 phase and promoted apoptosis in HCT116 cells. GSEA found that BGN might affect tumour progression via the mitogen-activated protein kinase (MAPK) signalling pathway. BGN might promote colon cancer progression via the MAPK signalling pathway and could be a potential target for future novel therapeutic strategies.

Exploring effects and mechanisms of Agrimoniae Herba-Coptidis Rhizoma containing serum on colorectal cancer cells via LAMP2A-mediated autophagy

This study investigated the effects of Agrimoniae Herba-Coptidis Rhizoma(XHC-HL)-medicated serum on the proliferation, migration, invasion, and apoptosis of human colorectal cancer HT29 and HCT116 cells via the autophagy mediated by lysosome-associated membrane protein type 2A(LAMP2A). Bioinformatics analysis was conducted to explore the role of LAMP2A in the development and progression of colorectal cancer. Western blot(WB) was used to detect the expression of LAMP2A protein in colorectal cancer cell lines. Lentiviral transfection was utilized to construct LAMP2A knockdown in HT29 and overexpression in HCT116 colorectal cancer cell models. Real-time fluorescence quantitative polymerase chain reaction(real-time qPCR) was performed to assess transfection efficiency. HT29 and HCT116 cells were treated with different concentrations of XHC-HL-medicated serum. The cell counting kit-8(CCK-8) assay was used to detect cell proliferation and determine the optimal concentration and duration of medicated serum intervention. HT29 cells were divided into a normal control(NC) group, an XHC-HL(medicated serum treatment) group, and an XHC-HL+shLAMP2A(medicated serum treatment+LAMP2A knockdown) group. HCT116 cells were divided into a NC group, an XHC-HL group, and an XHC-HL+LAMP2A(medicated serum treatment+LAMP2A overexpression) group. CCK-8 was used to measure cell viability. Colony formation assay was employed to assess cell proliferation ability. Scratch and Transwell migration assays were conducted to evaluate cell migration ability, and Transwell invasion assay was used to detect cell invasion ability. Flow cytometry was adopted to determine apoptosis rates. WB and real-time qPCR were employed to detect the effect of XHC-HL on the protein and mRNA expression of LAMP2A, heat shock cognate protein 70(HSC70), heat shock protein 90(HSP90), and glyceraldehyde-3-phosphate dehydrogenase(GAPDH) in colorectal cancer cells. Differential expression analysis revealed that LAMP2A expression was significantly higher in colorectal cancer patients compared to that in normal controls. Survival analysis indicated that the key molecule of chaperone-mediated autophagy(CMA), LAMP2A, was closely associated with colorectal cancer progression. Gene set enrichment analysis showed that patients with high LAMP2A expression significantly upregulated tumor progression-related signaling pathways such as angiogenesis and immune suppression. Immune infiltration analysis found that patients with high LAMP2A expression had fewer CD8 T cell infiltrations in their tumor microenvironment. XHC-HL-medicated serum inhibited the viability of HT29 and HCT116 cells, with the optimal intervention concentration and duration being 20% and 48 hours, respectively. Compared to the NC group, XHC-HL inhibited the proliferation, migration, and invasion of HT29 and HCT116 cells, and induced apoptosis. The medicated serum treatment with LAMP2A knockdown further inhibited colorectal cancer cell proliferation, invasion, and migration, and promoted apoptosis, whereas overexpression of LAMP2A reversed the inhibitory effects of the medicated serum on proliferation, migration, and invasion, and reduced apoptosis rates. XHC-HL-medicated serum inhibited CMA by upregulating the protein and mRNA expression of LAMP2A, HSC70, and HSP90 and downregulating substrate protein GAPDH expression via the autophagy mediated by LAMP2A. In conclusion, XHC-HL-medicated serum inhibits the proliferation, migration, and invasion of colorectal cancer cells and induces apoptosis by downregulating the expression of the key CMA molecule LAMP2A and inhibiting CMA activity.