scholarly journals Research of the mechanism on miRNA193 in exosomes promotes cisplatin resistance in esophageal cancer cells

2019 ◽  
Author(s):  
Shifeng Shi ◽  
Xin Huang ◽  
Xiao Ma ◽  
Xiaoyan Zhu ◽  
Qinxian Zhang
Keyword(s):  
Cell Cycle ◽  
Drug Resistance ◽  
Esophageal Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cisplatin Resistance ◽  
High Expression ◽  
Drug Resistant ◽  
Cellular Resistance ◽  
Esophageal Cancer Cells

AbstractPurposeChemotherapy resistance of esophageal cancer is a key factor affecting the postoperative treatment of esophageal cancer. Among the media that transmit signals between cells, the exosomes secreted by tumor cells mediate information transmission between tumor cells, which can make sensitive cells obtain resistance. Although some cellular exosomes play an important role in tumor’s acquired drug resistance, the related action mechanism is still not explored specifically.MethodsTo elucidate this process, we constructed a cisplatin-resistant esophageal cancer cell line, and proved that exosomes conferring cellular resistance in esophageal cancer can promote cisplatin resistance in sensitive cells. Through high-throughput sequencing analysis of the exosome and of cells after stimulation by exosomes, we determined that the miRNA193 in exosomes conferring cellular resistance played a key role in sensitive cells acquiring resistance to cisplatin. In vitro experiments showed that miRNA193 can regulate the cell cycle of esophageal cancer cells and inhibit apoptosis, so that sensitive cells can acquire resistance to cisplatin. An in vivo experiment proved that miRNA193 can promote tumor proliferation through the exosomes, and provide sensitive cells with slight resistance to cisplatin.ResultsSmall RNA sequencing of exosomes showed that exosomes in drug-resistant cells have 189 up-regulated and 304 down-regulated miRNAs; transcriptome results showed that drug-resistant cells treated with drug-resistant cellular exosomes have 3446 high-expression and 1709 low-expression genes; correlation analysis showed that drug-resistant cellular exosomes mainly affect the drug resistance of sensitive cells through paths such as cytokine–cytokine receptor interaction, and the VEGF and Jak-STAT signaling pathways; miRNA193, one of the high-expression miRNAs in drug-resistant cellular exosomes, can promote drug resistance by removing cisplatin’s inhibition of the cell cycle of sensitive cells.ConclusionSensitive cells can become resistant to cisplatin through acquired drug-resistant cellular exosomes, and miRNA193 can make tumor cells acquire cisplatin resistance by regulating the cell cycle.

scholarly journals The involvement of MCTP1 in the drug-resistance of esophageal cancer cells

2020 ◽  
Author(s):  
Lingsuo Kong ◽  
Ran Wei ◽  
Wan Yang ◽  
Lanren Chen ◽  
Liting Qian
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Esophageal Cancer ◽  
Effective Treatment ◽  
Cancer Cells ◽  
Cell Lines ◽  
Drug Resistant ◽  
Proliferation And Apoptosis ◽  
Ec Cells ◽  
Esophageal Cancer Cells

Abstract Background: Accumulating studies demonstrated that drug-resistance remains a great obstacle for the effective treatment of cancers. Esophageal cancer (EC) is still one of the most common cancers worldwide, which also suffers from drug-resistance during clinical treatment. Methods: We performed the drug-resistance profiling assays and identified several drug-resistant and drug-sensitive EC cell lines. The following methylation sequencing showed that the MCTP1 gene is hypermethylated in the drug-resistant EC cells. Results: As a result, the expression of MCTP1 is down-regulated in the drug-resistant EC cells. Down-regulation of MCTP1 also affects the cell proliferation and apoptosis of EC cells, as revealed by the cell proliferation and apoptosis assays. Further investigations proposed two signaling pathways that might involve in the MCTP1-mediated drug-resistance of EC cell. Conclusions: All these results suggested that MCTP1 is associated with the drug-resistance of EC cells, which has implications for further design of new biomarker of EC treatment.

scholarly journals EMT and Cancer Cell Stemness Associated With Chemotherapeutic Resistance in Esophageal Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaojie Liu ◽  
Mingjing He ◽  
Linlin Li ◽  
Xiya Wang ◽  
Shuhua Han ◽  
...  
Keyword(s):  
Stem Cells ◽  
Drug Resistance ◽  
Esophageal Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Colony Formation ◽  
Cancer Drug ◽  
Drug Resistant ◽  
Esophageal Cancer Cells ◽  
Resistant Cells

Drug resistance often occurs after chemotherapy in esophageal cancer patients, leading to cancer metastasis and recurrence. However, the relationship among cancer cell migration, recurrence and drug resistance in esophageal cancer drug-resistant cells has not been clearly explained. In this study, we constructed paclitaxel (PTX)-resistant esophageal cancer cells to explore the causes of drug resistance and poor prognosis after chemotherapy in esophageal cancer. Colony formation assay was used to evaluate the difference of colony formation between parental cells and drug resistance cells. Microsphere formation assay was used to examine the phenotype of stem cells. Wound healing and Transwell assays were used to detect the migration ability of drug-resistant cells. Western blotting and immunofluorescence assays were used to explore the mechanisms. Finally, we used nude mouse xenograft model to explore the tumor characteristics and the expression of relative proteins to verify our findings in vivo. Our study demonstrated that the cancer cell stemness characteristics exist in drug-resistant esophageal cancer cells, that expressed the biomarkers of stem cells and were prone to epithelial-mesenchymal transition (EMT). Our results suggested that the expression of EMT biomarkers and stemness-related proteins increased in esophageal cancer cells after continuously using chemotherapeutic drugs for a period of time. This study indicated that simultaneously targeting EMT and stemness could be a better strategy for the treatment of esophageal cancer drug resistance.

scholarly journals Metabolic Reprogramming of Chemoresistant Cancer Cells and the Potential Significance of Metabolic Regulation in the Reversal of Cancer Chemoresistance

Metabolites ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 289 ◽  
Author(s):  
Xun Chen ◽  
Shangwu Chen ◽  
Dongsheng Yu
Keyword(s):  
Drug Resistance ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Metabolic Regulation ◽  
Metabolic Response ◽  
Pentose Phosphate ◽  
Metabolic Reprogramming ◽  
Acid Oxidation ◽  
Drug Resistant ◽  
Chemotherapy Drugs

Metabolic reprogramming is one of the hallmarks of tumors. Alterations of cellular metabolism not only contribute to tumor development, but also mediate the resistance of tumor cells to antitumor drugs. The metabolic response of tumor cells to various chemotherapy drugs can be analyzed by metabolomics. Although cancer cells have experienced metabolic reprogramming, the metabolism of drug resistant cancer cells has been further modified. Metabolic adaptations of drug resistant cells to chemotherapeutics involve redox, lipid metabolism, bioenergetics, glycolysis, polyamine synthesis and so on. The proposed metabolic mechanisms of drug resistance include the increase of glucose and glutamine demand, active pathways of glutaminolysis and glycolysis, promotion of NADPH from the pentose phosphate pathway, adaptive mitochondrial reprogramming, activation of fatty acid oxidation, and up-regulation of ornithine decarboxylase for polyamine production. Several genes are associated with metabolic reprogramming and drug resistance. Intervening regulatory points described above or targeting key genes in several important metabolic pathways may restore cell sensitivity to chemotherapy. This paper reviews the metabolic changes of tumor cells during the development of chemoresistance and discusses the potential of reversing chemoresistance by metabolic regulation.

scholarly journals Gypenoside L Inhibits Proliferation of Liver and Esophageal Cancer Cells by Inducing Senescence

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1054 ◽  
Author(s):  
Jingxin Ma ◽  
Xiaopeng Hu ◽  
Chenghui Liao ◽  
Haitao Xiao ◽  
Qinchang Zhu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Esophageal Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Inhibitory Effect ◽  
Cancer Cell Growth ◽  
Therapeutic Drugs ◽  
Cycle Arrest ◽  
Chemical Inhibitors ◽  
Esophageal Cancer Cells

Senescence is an irreversible state of cell cycle arrest that can be triggered by multiple stimuli, such as oxygen reactive species and DNA damage. Growing evidence has proven that senescence is a tumor-suppressive approach in cancer treatment. Therefore, developing novel agents that modulate senescence may be an alternative strategy against cancer. In our study, we investigated the inhibitory effect of gypenoside L (Gyp-L), a saponin isolated from Gynostemma pentaphyllum, on cancer cell growth. We found that Gyp-L increased the SA-β-galactosidase activity, promoted the production of senescence-associated secretory cytokines, and inhibited cell proliferation of human liver and esophageal cancer cells. Moreover, Gyp-L caused cell cycle arrest at S phase, and activated senescence-related cell cycle inhibitor proteins (p21 and p27) and their upstream regulators. In addition, Gyp-L activated p38 and ERK MAPK pathways and NF-κB pathway to induce senescence. Consistently, adding chemical inhibitors efficiently counteracted the Gyp-L-mediated senescence, growth inhibition, and cell cycle arrest in cancer cells. Furthermore, treatment with Gyp-L, enhanced the cytotoxicity of clinic therapeutic drugs, including 5-fluorouracil and cisplatin, on cancer cells. Overall, these results indicate that Gyp-L inhibits proliferation of cancer cells by inducing senescence and renders cancer cells more sensitive to chemotherapy.

Effect of miR-214 on Proliferation, Cell Cycle and Apoptosis of Esophageal Cancer Cells

2021 ◽  
Vol 11 (2) ◽  
pp. 315-319
Author(s):  
Yanfeng Wang ◽  
Hongling Gao ◽  
Hao Wang ◽  
Enguang Lin ◽  
Zhao Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Esophageal Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Real Time Pcr ◽  
Cell Number ◽  
G1 Phase ◽  
Specific Mechanism ◽  
Esophageal Cancer Cells

Esophageal cancer seriously affects human health. miR-214 involves in esophageal cancer, but its specific mechanism has not been completely elucidated. Our study investigated miR-214’s role in esophageal cancer. Eca109 cells were transfected with miR-214 inhibitor/NC was transfected into Eca109 cells followed by analysis of miR-214 level by real-time PCR, cell proliferation by CCK8 assay, cell apoptosis and cell cycle and PTEN level by Western blot. miR-214 was significantly upregulated in Eca109 cells (P < 0.01) with downregulated PTEN (P < 0.05). miR-214 inhibitor significantly upregulated PTEN, decreased cell number, increased apoptosis and cells in G1 phase (P < 0.05). PTEN was a target of miR-214. miR-214 affects esophageal cancer cells by targeting PTEN.

scholarly journals Research of the mechanism on miRNA193 in exosomes promotes cisplatin resistance in esophageal cancer cells

PLoS ONE ◽  
2020 ◽  
Vol 15 (5) ◽  
pp. e0225290 ◽  
Author(s):  
Shifeng Shi ◽  
Xin Huang ◽  
Xiao Ma ◽  
Xiaoyan Zhu ◽  
Qinxian Zhang
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Esophageal Cancer Cells
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