MicroRNA‐195 Chemosensitizes Colon Cancer Cells to the Chemotherapeutic Drug Doxorubicin by Targeting the First Binding Site of BCL2L2 mRNA

Zhao, Liang; Zhang, Pengzhi; Wang, Juan; Xu, Ning; Mi, Wenjuan; Jiang, Xingwang; Zhang, Changming; Qu, Juan

doi:10.1002/jcp.24366

Cited by 71 publications

(47 citation statements)

References 51 publications

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“…At present, the application of doxorubicin, a DNA‐intercalating anthracycline antibiotic, in combination with other anti‐tumor drugs exhibits good therapeutic effects against late‐stage CC (Qu et al, ). However, chemoresistance is a frequent event and inhibits the clinical application of chemotherapy drugs.…”

Section: Discussionmentioning

confidence: 99%

Forkhead box O3 promotes colon cancer proliferation and drug resistance by activating MDR1 expression

Gao

Liu

et al. 2019

Molec Gen & Gen Med

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Background Globally, colon cancer (CC) is the third reason of tumor‐related deaths. Previous reports indicate that Forkhead box O3 (FOXO3) is involved in the development of various tumors and may have different effects depending upon the types of tumors. Hence, this study was to examine the effects of FOXO3 on CC cells and uncover the possible mechanisms. Methods MTT and cell count assay were applied to analyze the viability of transfected CC cells. rVista, dual luciferase reporter assay, and chromatin immunoprecipitation assay were used to identify the downstream target of FOXO3 in HCT116 cells. The mRNA and protein abundance of FOXO3 and MDR1 were determined by quantitative PCR and Western blot, respectively. Results Forkhead box O3 stimulated the proliferation of both HCT116 and DLD1 cells. Moreover, FOXO3 overexpression inhibited doxorubicin sensitivity of HCT116 cells, while the knockout of FOXO3 by FOXO3 shRNA restored the doxorubicin sensitivity in doxorubicin‐resistant HCT116 DR cells. Next, we found that FOXO3 directly bound to the promoter of MDR1 and enhanced MDR1 expression in HCT116 cells. MDR1 overexpression enhanced the viability and doxorubicin resistance of CC cells. Besides, MDR1 overexpression plasmid significantly abrogated the decrease in cell proliferation and resistance of HCT116 cells to doxorubicin caused by FOXO3 knockout. Conclusion Forkhead box O3 exhibited promotive effects on the proliferation and doxorubicin resistance in CC cells via targeting MDR1.

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Section: Discussionmentioning

confidence: 99%

Forkhead box O3 promotes colon cancer proliferation and drug resistance by activating MDR1 expression

Gao

Liu

et al. 2019

Molec Gen & Gen Med

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“…Moreover, Liu et al and Chen et al proved that EZH2 promoted the progression and invasion of human gastric cancer [26, 27]. BCL2L2 was determined to promote tumorigenicity and invasion in human glioblastoma, non-small-cell lung cancer, and colon cancer [28–30]. CDH2 was reported to be related to the epithelial-mesenchymal transition (EMT) in non-small-cell lung cancer [31].…”

Section: Discussionmentioning

confidence: 99%

Role of ARPC2 in Human Gastric Cancer

Zhang

Liu

et al. 2017

Mediators of Inflammation

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Gastric cancer continues to be the second most frequent cause of cancer deaths worldwide. However, the exact molecular mechanisms are still unclear. Further research to find potential targets for therapy is critical and urgent. In this study, we found that ARPC2 promoted cell proliferation and invasion in the human cancer cell line MKN-28 using a cell total number assay, MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) assay, cell colony formation assay, migration assay, invasion assay, and wound healing assay. For downstream pathways, CTNND1, EZH2, BCL2L2, CDH2, VIM, and EGFR were upregulated by ARPC2, whereas PTEN, BAK, and CDH1 were downregulated by ARPC2. In a clinical study, we examined the expression of ARPC2 in 110 cases of normal human gastric tissues and 110 cases of human gastric cancer tissues. ARPC2 showed higher expression in gastric cancer tissues than in normal gastric tissues. In the association analysis of 110 gastric cancer tissues, ARPC2 showed significant associations with large tumor size, lymph node invasion, and high tumor stage. In addition, ARPC2-positive patients exhibited lower RFS and OS rates compared with ARPC2-negative patients. We thus identify that ARPC2 plays an aneretic role in human gastric cancer and provided a new target for gastric cancer therapy.

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“…Dong et al׳s study 128 found that miR-21 was involved in gemcitabine resistance by directly upregulating BCL-2 expression in pancreatic cancer cells. Other miRNAs found to directly target BCL-2 using Western blot and luciferase activity assays include miR-497 129 , miR-200bc/429 cluster 130 , miR-1915 131 , miR-214 132 miR-195 133 , and miR-205 134 .…”

Section: Aberrant Expression Of Mirnas and Cancer Drug Resistancementioning

confidence: 99%

Regulation of multidrug resistance by microRNAs in anti-cancer therapy

An¹,

Sarmiento

Tan

et al. 2017

Acta Pharmaceutica Sinica B

166

132

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Multidrug resistance (MDR) remains a major clinical obstacle to successful cancer treatment. Although diverse mechanisms of MDR have been well elucidated, such as dysregulation of drugs transporters, defects of apoptosis and autophagy machinery, alterations of drug metabolism and drug targets, disrupti on of redox homeostasis, the exact mechanisms of MDR in a specific cancer patient and the cross-talk among these different mechanisms and how they are regulated are poorly understood. MicroRNAs (miRNAs) are a new class of small noncoding RNAs that could control the global activity of the cell by post-transcriptionally regulating a large variety of target genes and proteins expression. Accumulating evidence shows that miRNAs play a key regulatory role in MDR through modulating various drug resistant mechanisms mentioned above, thereby holding much promise for developing novel and more effective individualized therapies for cancer treatment. This review summarizes the various MDR mechanisms and mainly focuses on the role of miRNAs in regulating MDR in cancer treatment.

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MicroRNA‐195 Chemosensitizes Colon Cancer Cells to the Chemotherapeutic Drug Doxorubicin by Targeting the First Binding Site of BCL2L2 mRNA

Cited by 71 publications

References 51 publications

Forkhead box O3 promotes colon cancer proliferation and drug resistance by activating MDR1 expression

Forkhead box O3 promotes colon cancer proliferation and drug resistance by activating MDR1 expression

Role of ARPC2 in Human Gastric Cancer

Regulation of multidrug resistance by microRNAs in anti-cancer therapy

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