Increased miR‐323a induces bladder cancer cell apoptosis by suppressing c‐Met

Qiu, Jun; Zeng, Furen; Fang, Yi; Li, Jian; Xiao, Sheng-Ying

doi:10.1002/kjm2.12091

Cited by 7 publications

(7 citation statements)

References 28 publications

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“…24 Also, in bladder cancer, miR-323a overexpression elicits tumor cell apoptosis through targeting c-Met. 25 In this study, miR-323a showed to be downregulated within pancreatic cancer tissue samples and cells based on online datasets and experimental analyses, suggesting its potential role in suppressing pancreatic cancer. Indeed, miR-323a overexpression significantly suppressed pancreatic carcinoma cell proliferation and colony formation.…”

Section: Discussionmentioning

confidence: 64%

Tumor‐suppressive miR‐323a inhibits pancreatic cancer cell proliferation and glycolysis through targeting HK‐2

Wei

Wang

Liang

et al. 2022

Pathology International

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Pancreatic ductal adenocarcinoma (PDAC) accounts for more than 85% of all malignant pancreatic exocrine tumors and is one of the main causes of cancer‐related fatalities. PDAC is characterized by a high glycolytic rate to ensure its survival as a result of hypovascularization and the desmoplastic reaction. In this study, microRNA 323a (miR‐323a) was shown to be downregulated within pancreatic cancer tissues and cells, and enriched in the glucose metabolism pathway. In vitro, overexpression of miR‐323a suppressed cell viability, DNA synthesis, and colony formation; in vivo, miR‐323a overexpression suppressed the tumor growth within a xenograft mouse model. Regarding cellular glycolysis, miR‐323a overexpression decreased glucose‐6‐phosphate levels, inhibited glucose uptake, and reduced lactate and adenosine triphosphate production. miR‐323a was found to directly target hexokinase 2 (HK‐2) and negatively regulated HK‐2 expression. HK‐2 overexpression exerted oncogenic effects on pancreatic cancer cells and promoted cellular glycolysis; more importantly, HK‐2 overexpression partially eliminated the effects of miR‐323a overexpression. In conclusion, miR‐323a is downregulated within pancreatic cancer and serves as a tumor‐suppressive miRNA through inhibiting cancer cell proliferation and glycolysis. miR‐323a exerts its tumor‐suppressive effects through targeting HK‐2.

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Section: Discussionmentioning

confidence: 64%

Tumor‐suppressive miR‐323a inhibits pancreatic cancer cell proliferation and glycolysis through targeting HK‐2

Wei

Wang

Liang

et al. 2022

Pathology International

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“…There were significant miR-323a downregulations in BCa tissues and cell lines. MiR-323a induced apoptosis of BCa cells through c-MET inhibition [99]. MiR-409-3p downregulation was also observed in BCa tissues and cell lines.…”

Section: Class V Vii and Viii Receptors Of Tyrosine Kinasesmentioning

confidence: 86%

MicroRNAs as the critical regulators of protein kinases in prostate and bladder cancers

Zangoue

Zangouei

Mojarrad

et al. 2021

Egypt J Med Hum Genet

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Background Bladder cancer (BCa) and prostate cancer (PCa) are frequent urothelial and genital malignancies with a high ratio of morbidity and mortality which are more common among males. Since BCa and PCa cases are mainly diagnosed in advanced stages with clinical complications, it is required to introduce the efficient early detection markers. Protein kinases are critical factors involved in various cellular processes such as cell growth, motility, differentiation, and metabolism. Deregulation of protein kinases can be frequently observed through the neoplastic transformation and tumor progression. Therefore, kinases are required to be regulated via different genetic and epigenetic processes. MicroRNAs (miRNAs) are among the critical factors involved in epigenetic regulation of protein kinases. Since miRNAs are noninvasive and more stable factors in serum and tissues compared with mRNAs, they can be used as efficient diagnostic markers for the early detection of PCa and BCa. Main body In present review, we have summarized all of the reported miRNAs that have been associated with regulation of protein kinases in bladder and prostate cancers. Conclusions For the first time, this review highlights the miRNAs as critical factors in regulation of protein kinases during prostate and bladder cancers which paves the way of introducing a noninvasive kinase-specific panel of miRNAs for the early detection of these malignancies. It was observed that the class VIII receptors of tyrosine kinases and non-receptor tyrosine kinases were the most frequent targets for the miRNAs in bladder and prostate cancers, respectively.

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“…A large number of studies have shown that miRNAs regulate more than one-third of all human genes in a sequence-specific manner [27][28][29][30]. Aberrant regulation of miRNAs functionally promotes the occurrence and development of different human cancers by regulating the degradation or translation of mRNAs [31][32][33][34].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-323a-3p Negatively Regulates NEK6 in Colon Adenocarcinoma Cells

Hong

Chen

Pan

et al. 2022

Journal of Oncology

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Objective. The activity of NEK6 is enhanced in several cancer cells, including colon adenocarcinoma (COAD) cells. However, there are few reports on the microRNA (miRNA/miR) regulation of NEK6. In this study, we aimed to investigate the effects of miRNAs targeting NEK6 in COAD cells. Methods. Public data and online analysis sites were used to analyze the expression levels of NEK6 and miR-323a-3p in COAD tissues as well as the relationship between NEK6 or miR-323a-3p levels and survival in patients with COAD and to predict miRNAs targeting NEK6. Real-time polymerase chain reaction and western blotting were performed to determine the levels of NEK6 and miR-323a-3p in COAD cells. The targeting of NEK6 by miR-323a-3p was verified using a dual-luciferase reporter assay. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, 5-ethynyl-2′-deoxyuridine assay, propidium iodide (PI) staining, annexin V-fluorescein isothiocyanate/PI staining, and transwell assay were employed to test the proliferation, apoptosis, migration ability, and invasiveness of COAD cells. Results. In COAD cells, NEK6 was highly expressed, whereas miR-323a-3p was expressed at low levels and negatively regulated NEK6. Upregulating the level of miR-323a-3p impaired the proliferation, migration, and invasion of COAD cells and promoted apoptosis, whereas supplementing NEK6 alleviated the damage of the proliferation, migration, and invasion of COAD cells caused by miR-323a-3p and inhibited miR-323a-3p-induced apoptosis. These findings indicate that miR-323a-3p regulates the proliferation, migration, invasion, and apoptosis of COAD cells by targeting NEK6. Conclusion. miR-323a-3p downregulates NEK6 in COAD cells; this provides a novel basis for further understanding the occurrence and development of COAD.

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Increased miR‐323a induces bladder cancer cell apoptosis by suppressing c‐Met

Cited by 7 publications

References 28 publications

Tumor‐suppressive miR‐323a inhibits pancreatic cancer cell proliferation and glycolysis through targeting HK‐2

Tumor‐suppressive miR‐323a inhibits pancreatic cancer cell proliferation and glycolysis through targeting HK‐2

MicroRNAs as the critical regulators of protein kinases in prostate and bladder cancers

MicroRNA-323a-3p Negatively Regulates NEK6 in Colon Adenocarcinoma Cells

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