Up‐regulation of miR‐497 confers resistance to temozolomide in human glioma cells by targeting <scp>mTOR</scp>/Bcl‐2

Zhu, Dan; Tu, Ming; Zeng, Bo; Cai, Lin; Zheng, Wenjie; Su, Zhipeng; Yu, Zhengquan

doi:10.1002/cam4.987

Cited by 44 publications

(31 citation statements)

References 29 publications

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“…Bcl-2 is a protein involved in modulating cell death through suppressing apoptosis and promoting cell survival. In several types of cancer, Bcl-2 is reported to be upregulated (23,24). Its expression is also considered to be regulated by multiple miRNAs, including miR-497.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-497 inhibits multiple myeloma growth and increases susceptibility to bortezomib by targeting Bcl-2

et al. 2018

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Multiple myeloma (MM) is a common severe hematopoietic malignancy occuring in aged population. MicroRNA (miR)-497 was previously reported to contribute to the apoptosis of other cell types, presumably through targeting B-cell lymphoma 2 (Bcl-2). In the present study, miRNA and protein expression levels were detected by reverse transcription-quantitative polymerase chain reaction and western blot analyses, respectively. The cell proliferation and viability was measured using 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide and plate clonality assays, and the cell growth cycle was measured with a flow cytometer. Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end-labeling, Annexin V and caspase-3 activity assays were performed to examine the cell apoptotic rates. The results showed that miR-497 was markedly decreased, whereas Bcl-2 was enhanced in MM tissues and cell lines. miR-497 targeted Bcl-2 and affected its downstream apoptosis-related genes. The overexpression of miR-497 promoted MM cell apoptosis through cell cycle arrest, and decreased colony genesis ability and viability. In addition, miR-497 increased the sensitivity of MM cells to bortezomib. Taken together, miR-497 suppressed MM cell proliferation and promoted apoptosis by directly targeting Bcl-2 and altering the expression of downstream apoptosis-related proteins. The combination of miR-497 and bortezomib may enhance drug sensitivity, serving as a potentially available therapeutic method for MM.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-497 inhibits multiple myeloma growth and increases susceptibility to bortezomib by targeting Bcl-2

et al. 2018

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“…For example, miR-24 can induce chemotherapy resistance and hypoxic advantage in breast cancer through the downregulation of factor inhibiting HIF-1 ( 24 ). miR-497 is significantly correlated with temozolomide-resistance in glioma cells by regulating the insulin-like growth factor 1 receptor/insulin receptor substrate 1 pathway ( 25 ). miR-93 is known to affect metastatic spread in breast carcinoma through the regulation of protein kinase WNK1 ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

miR-494 inhibits cell proliferation and metastasis via targeting of CDK6 in osteosarcoma

Yuan

Wei

Liu

et al. 2017

Molecular Medicine Reports

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Tumorigenesis is a multistep process involving various cell growth-associated factors. Accumulated evidence indicates that the disordered regulation of microRNAs (miRNAs) contributes to tumorigenesis. However, the detailed mechanism underlying the involvement of miRNAs in oncogenesis remains to be fully elucidated. In the present study, the repressed expression of microRNA (miR)-494 was identified in 18 patients with osteosarcoma (OS) and OS cell lines, compared with corresponding controls. To determine whether deregulated miR-494 exerts tumor-suppressive effects in the development of OS, the effects of miR-494 on cell proliferation and metastasis were evaluated. It was found that the restoration of miR-494 in MG-63 and U2OS cells led to inhibited cell proliferation and attenuated migratory propensity in vitro, determined through analysis using MTT, colony formation and Transwell assays. In addition, overexpression of miR-494 markedly suppressed the tumor volume and weight in vivo. In accordance, the ectopic expression of miR-494 induced cell cycle arrest at the G1/S phase in OS cells. Bioinformatics analysis and luciferase reporter assays were performed to investigate the potential regulatory role of miR-494, the results of which indicated that miR-494 directly targeted cyclin-dependent kinase 6 (CDK6). Of note, the data obtained through reverse transcription-quantitative polymerase chain reaction and western blot analyses suggested that the elevated expression of miR-494 resulted in reduced mRNA and protein expression levels of CDK6. Taken together, these findings indicated that the miR-494/CDK6 axis has a significant tumor-suppressive effect on OS, and maybe a diagnostic and therapeutic target for the treatment of OS.

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“…However, the impact of miR-497 is reversed in glioma. Upregulation of miR-497 has been found in human glioma and it enables cells to develop resistance to temozolomide treatment by targeting mTOR and Bcl-2, indicating the diverse or even oppose functions of miR-497 in cancer [69].…”

Section: Mir-497mentioning

confidence: 99%

Non-Coding RNAs in IGF-1R Signaling Regulation: The Underlying Pathophysiological Link between Diabetes and Cancer

Chen

Chi

et al. 2019

Cells

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The intricate molecular network shared between diabetes mellitus (DM) and cancer has been broadly understood. DM has been associated with several hormone-dependent malignancies, including breast, pancreatic, and colorectal cancer (CRC). Insulin resistance, hyperglycemia, and inflammation are the main pathophysiological mechanisms linking DM to cancer. Non-coding RNAs (ncRNAs), particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), are widely appreciated as pervasive regulators of gene expression, governing the evolution of metabolic disorders, including DM and cancer. The ways ncRNAs affect the development of DM complicated with cancer have only started to be revealed in recent years. Insulin-like growth factor 1 receptor (IGF-1R) signaling is a master regulator of pathophysiological processes directing DM and cancer. In this review, we briefly summarize a number of well-known miRNAs and lncRNAs that regulate the IGF-1R in DM and cancer, respectively, and further discuss the potential underlying molecular pathogenesis of this disease association.

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Up‐regulation of miR‐497 confers resistance to temozolomide in human glioma cells by targeting mTOR/Bcl‐2

Cited by 44 publications

References 29 publications

MicroRNA-497 inhibits multiple myeloma growth and increases susceptibility to bortezomib by targeting Bcl-2

MicroRNA-497 inhibits multiple myeloma growth and increases susceptibility to bortezomib by targeting Bcl-2

miR-494 inhibits cell proliferation and metastasis via targeting of CDK6 in osteosarcoma

Non-Coding RNAs in IGF-1R Signaling Regulation: The Underlying Pathophysiological Link between Diabetes and Cancer

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