MicroRNA-1297 inhibits proliferation and promotes apoptosis in gastric cancer cells by downregulating CDC6 expression

Zhang, Xiangqian; Zhang, Min; Guo, Qingqing; Hu, Xiaoyi; Zhao, Zhenghao; Ni, Lei; Liu, Liying; Wang, Xiaofei; Wang, Zhenzhen; Tong, Dongdong; Chang, Sue; Cao, Ye; Huang, Chen

doi:10.1097/cad.0000000000000776

Cited by 18 publications

(16 citation statements)

References 34 publications

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“…Wang et al reported that introduction of miR‐32‐5p directly targeted KLF2 to promote cell proliferation and migration of GC via activating PI3K/AKT signalling pathway . Zhang et al indicated that up‐regulation of miR‐1297 inhibited GC cell proliferation and induced GC cell apoptosis by directly regulating the CDC6 expression . Numerous studies have found that miR‐665 not only affected cell proliferation but also was closely associated with prognosis in cancers including breast cancer, hepatocellular carcinoma, acute lymphoblastic leukaemia, colorectal cancer, cervical cancer, and ovarian cancer …”

Section: Discussionmentioning

confidence: 99%

“…Thus, miRNAs are thought to be markers of cancers diagnosis, progression, and prognosis . Many human miRNAs have been confirmed to be dysregulated in GC, including miR‐32‐5p, miR‐544a, miR‐1297, miR‐625, and miR‐383‐5p . Up to now, miR‐665 has been reported to function as an oncogene in breast cancer, hepatocellular carcinoma, acute lymphoblastic leukaemia, or function as a tumour suppressor in colorectal cancer, cervical cancer, and ovarian cancer; the functions of miR‐665 in GC were rare unexplored previously.…”

Section: Introductionmentioning

confidence: 99%

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microRNA‐665 is down‐regulated in gastric cancer and inhibits proliferation, invasion, and EMT by targeting PPP2R2A

Zhang¹,

Wang

Yi³

et al. 2020

Cell Biochemistry & Function

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Recently, microRNA-665 (miR-665) has been reported to function as both tumour suppressor and oncogene in several cancer types, including gastric cancer, hepatocellular cancer, and lung cancer. However, the biological function of miR-665 and its precise mechanisms in gastric cancer (GC) have not been well clarified. The aim of this study was to study the roles of miR-665/PPP2R2A axis in GC. The levels of PPP2R2A and miR-665 were detected by quantitative PCR assay in GC tissues and cell lines. Moreover, the biological roles of miR-665 and PPP2R2A in GC cells were assessed by cell proliferation, invasion, and epithelial-mesenchymal transition (EMT).The mRNA and protein levels of PPP2R2A were determined by using quantitative PCR and Western blotting assays. Luciferase assays were used to confirm that PPP2R2A was one target of miR-665. In this study, the miR-665 level was dramatically reduced in GC tissues and cell lines, and the PPP2R2A expression was significantly enhanced. What is more, the PPP2R2A expression was negatively related to the miR-665 level in GC tissues. Furthermore, up-regulation of miR-665 obviously restrained GC cells proliferation, invasion, and EMT. We confirmed that miR-665 could directly target PPP2R2A by luciferase reporter assay. Besides, knockdown of PPP2R2A also could markedly inhibit the proliferation, invasion and EMT of GC cells.Finally, overexpression of miR-665 in GC cells partially reversed the promoted effects of PPP2R2A up-regulation. Overexpression of miR-665 restrained GC cells proliferation, invasion and EMT via regulation of PPP2R2A.Significance of the study miR-665 has been reported to function as oncogene or tumour suppressor in different cancers. However, the precise roles of miR-665 in GC have not been elucidated. Our study for the first time demonstrated that miR-665 level was significantly down-regulated in GC. Additionally, miR-665 overexpression inhibited cell growth, invasion, and EMT of GC. Moreover, our data suggested a significant negative correlation between miR-665 and PPP2R2A expression in GC. MiR-665 suppressed GC cell proliferation, invasion, and EMT by directly targeting PPP2R2A, which suggested important roles for miR-665/PPP2R2A axis in the GC pathogenesis and its potential application in cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

microRNA‐665 is down‐regulated in gastric cancer and inhibits proliferation, invasion, and EMT by targeting PPP2R2A

Zhang¹,

Wang

Yi³

et al. 2020

Cell Biochemistry & Function

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show abstract

“…Increasing studies have reported that miRNAs were involved in regulating the biological behaviors of GC by the regulation of downstream genes. MiR-671-5p and miR-1297 repressed proliferation and promoted apoptosis of GC cells, respectively, by targeting URGCP [18] and CDC6 [35]. Additionally, miR-664a-3p contributed to the evolution of GC via targeting the Hippo pathway [29].…”

Section: Discussionmentioning

confidence: 99%

LncRNA NEAT1 promotes gastric cancer progression via miR-1294/AKT1 axis

Wang

et al. 2020

Open Medicine

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Long non-coding RNAs (lncRNAs) were reported to promote the development of gastric cancer (GC). Nuclear-enriched abundant transcript 1 (NEAT1) played a great role in diverse cancers, but the mechanism of NEAT1 in GC remains indistinct. NEAT1 and AKT1 were distinctly up-regulated and miR-1294 was down-regulated in GC tissues and cells. Cell proliferation and metastasis were refrained but apoptosis was promoted in GC cells after knockdown of NEAT1. NEAT1 negatively regulated miR-1294 expression, and the miR-1294 inhibitor reverted the si-NEAT1-induced effect on GC cells. NEAT1 modulated AKT1 expression through miR-1294, and the si-NEAT1-induced effect was relieved by AKT1. NEAT1 affected phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway via regulating miR-1294 and AKT1. NEAT1 could modulate cell proliferation, apoptosis, and metastasis in GC cells by regulating the PI3K/AKT/mTOR signaling pathway via the miR-1294/AKT1 axis, showing the great potential for NEAT1 as a valid biomarker in the progression and treatment of GC.

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“…In recent years, most human genome transcripts have been transcribed into non-coding RNAs, such as small non-coding RNAs (miRNAs). miRNAs do not encode any protein, but can regulate biological processes by inhibiting the expression level of target gene mRNA, thereby regulating the occurrence and progression of the disease (11)(12)(13). Studies have shown that miRNAs are differentially expressed in a variety of cancers, and differentially expressed miRNAs can be involved in the development and progression of cancer (14)(15)(16)(17), including colon cancer (18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of miR‑98 inhibiting tumor proliferation and invasion by targeting IGF1R in diabetic patients combined with colon cancer

Liu

Zhou

et al. 2020

Oncol Lett

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Expression level of miR-98 in diabetic colon cancer (CRC) tissues and the regulation mechanism of colon cancer cell proliferation and invasion ability were studied. Forty patients with type 2 diabetes mellitus complicated with colon cancer, 40 colon cancer patients, and 40 patients with diabetic colonoscopy were enrolled between January 2017 and January 2018. Real-time quantitative PCR was used to detect the expression level of miR-98. After SW480 cells were transfected with miR-98 mimics or control simulants, the proliferation of cancer cells was detected by MTT assay, and the invasion ability of cancer cells was detected by Transwell cell invasion assay. The dual luciferase assay was used to detect the binding relationship between miR-98 and IGF1R. Western blot analysis was used to detect the expression of IGF1R protein in tumor tissues of patients with diabetes mellitus and colon cancer. Compared with diabetic patients, the expression level of miR-98 was decreased in colon cancer patients. Compared with tumor tissues of colon cancer patients, the expression level of miR-98 was significantly decreased in diabetic colon cancer tissues. Compared with the commonly cultured colon cancer SW480 cells, the expression level of miR-98 was significantly decreased in SW480 cells cultured under high glucose conditions. Increased expression of miR-98 inhibits colon cancer cell proliferation and invasion. miR-98 can target and bind to IGF1R and inhibit its expression level. IGF1R is upregulated in diabetic colon cancer tissue. miR-98 inhibits proliferation and invasion of diabetic colon cancer by targeting IGF1R. The expression level of miR-98 in diabetic colon cancer tissues is lower than that in colon cancer tissues. miR-98 can inhibit the proliferation and invasion of colon cancer cells by targeting the target gene IGF1R. miR-98 may be a potential biological target for the treatment of patients with diabetes and colon cancer.

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MicroRNA-1297 inhibits proliferation and promotes apoptosis in gastric cancer cells by downregulating CDC6 expression

Cited by 18 publications

References 34 publications

microRNA‐665 is down‐regulated in gastric cancer and inhibits proliferation, invasion, and EMT by targeting PPP2R2A

microRNA‐665 is down‐regulated in gastric cancer and inhibits proliferation, invasion, and EMT by targeting PPP2R2A

LncRNA NEAT1 promotes gastric cancer progression via miR-1294/AKT1 axis

Mechanism of miR‑98 inhibiting tumor proliferation and invasion by targeting IGF1R in diabetic patients combined with colon cancer

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