MicroRNA 362-3p Reduces hERG-related Current and Inhibits Breast Cancer Cells Proliferation

Assiri, Abdullah; Mourad, Noha A.; Shao, Minghai; Kiel, Patrick J.; W, Liu; Skaar, Todd C.; Overholser, Brian R.

doi:10.21873/cgp.20147

Cited by 27 publications

(20 citation statements)

References 38 publications

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“…Furthermore, some studies have reported its pivotal effect on tumors. Assiri et al [25] revealed that miR-362-3p mediates the transcriptional regulation of the human ether-ago-go-related gene (hERG) and is associated with survival in breast cancer [25]. Christensen's study concluded that miR-362-3p may be a novel prognostic marker for colorectal cancer, and this study hypothesizes that the positive effects of augmented miR-362-3p expression may in part be mediated through hypothetical target protein 1 (PTPN1) [26].…”

Section: Discussionmentioning

confidence: 99%

miR-362-3p acts as a tumor suppressor by targeting SERBP1 in ovarian cancer

Cao

Xi-hong

2021

J Ovarian Res

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Background Ovarian cancer is the leading lethal gynecological cancer and is generally diagnosed during late-stage presentation. In addition, patients with ovarian cancer still face a low 5-year survival rate. Thus, innovative molecular targeting agents are required to overcome this disease. The present study aimed to explore the function of miR-362-3p and the underlying molecular mechanisms influencing ovarian cancer progression. Methods The expression levels of miR-362-3p were determined using qRT-PCR. Gain-of-function and loss-of-function methods were used to detect the effects of miR-362-3p on cell proliferation, cell migration, and tumor metastasis in ovarian cancer. A luciferase reporter assay was performed to confirm the potential target of miR-362-3p, and a rescue experiment was employed to verify the effect of miR-362-3p on ovarian cancer by regulating its target gene. Results miR-362-3p was significantly downregulated in ovarian cancer tissues and cell lines. In vitro, our data showed that miR-362-3p suppressed cell proliferation and migration. In vivo, miR-362-3p inhibited ovarian cancer growth and metastasis. Mechanistically, SERBP1 was identified as a direct target and functional effector of miR-362-3p in ovarian cancer. Moreover, SERBP1 overexpression rescued the biological function of miR-362-3p. Conclusions Our data reveal that miR-362-3p has an inhibitory effect on ovarian cancer. miR-362-3p inhibits the development and progression of ovarian cancer by directly binding its target gene SERBP1.

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Section: Discussionmentioning

confidence: 99%

miR-362-3p acts as a tumor suppressor by targeting SERBP1 in ovarian cancer

Cao

Xi-hong

2021

J Ovarian Res

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“…Through bioinformatics analysis, we found that miR-338-3P and miR-362-3P may be downstream target genes of SBF2-AS1. The tumour suppressor genes miR-338-3P-32 32 , 33 and miR-362-3P 34 , 35 are downregulated in many tumours such as ESCC. In this study, RIP and RNA-pull down experiments showed that SBF2-AS1 could directly target miR-338-3P and miR-362-3P, which confirmed the results of bioinformatics analysis.…”

Section: Discussionmentioning

confidence: 99%

The molecular mechanisms of the long noncoding RNA SBF2-AS1 in regulating the proliferation of oesophageal squamous cell carcinoma

Zha

Tie

et al. 2021

Sci Rep

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The long noncoding RNASBF2-AS1 can promote the occurrence and development of many kinds of tumours, but its role in oesophageal squamous cell carcinoma (ESCC) is unknown. We found that SBF2-AS1 was up-regulated in ESCC, and its expression was positively correlated with tumor size (P = 0.0001), but was not related to gender, age, TNM stage, histological grade, and lymphnode metastasis (P > 0.05). It was further found that the higher the expression of SBF2-AS1, the lower the survival rate. COX multivariate analysis showed that the expression of SBF2-AS1 was an independent prognostic factor. Functional experiments show that inhibition of SBF2-AS1 can inhibit the proliferation of ESCC through in vivo and in vitro, and overexpression of SBF2-AS1 can promote the proliferation of ESCC and inhibit its apoptosis. In mechanism, SBF2-AS1/miR-338-3P, miR-362-3P/E2F1 axis are involved in the regulation of ESCC growth. In general, SBF2-AS1 may be used as ceRNA to combine with miR-338-3P and miR-362-3P to up-regulate the expression ofE2F1, and ultimately play a role in promoting cancer. It may be used as a therapeutic target and a biomarker for prognosis.

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“…In gastric cancer, miR‐362‐3p is highly expressed and promotes the migration and invasion of gastric cancer cells by targeting CD82 22 . However, in renal cell carcinoma, breast cancer, lung adenocarcinoma, and colorectal cancer, miR‐362‐3p are all under‐expressed, and inhibit various biological behaviors of cells by regulating hERG, E2F1, USF2, and PTPN 8,9,23–25 . In CC, low expression of miR‐362‐3p is associated with poor prognosis, 11 and miR‐362‐3p inhibits proliferation through MCM5 and other targets 10 .…”

Section: Discussionmentioning

confidence: 99%

“…22 However, in renal cell carcinoma, breast cancer, lung adenocarcinoma, and colorectal cancer, miR-362-3p are all under-expressed, and inhibit various biological behaviors of cells by regulating hERG, E2F1, USF2, and PTPN. 8,9,[23][24][25] In CC, low expression of miR-362-3p is associated with poor prognosis, 11 and miR-362-3p inhibits proliferation through MCM5 and other targets. 10 This may be the reason why the effect of miR-362 mimics is not weaker than siBAP on cell biological behaviors in our research results.…”

Section: Discussionmentioning

confidence: 99%

MiR‐362 suppresses cervical cancer progression via directly targeting BAP31 and activating TGFβ/Smad pathway

et al. 2020

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BAP31 (B‐cell receptor‐associated protein 31) is an important regulator of intracellular signal transduction and highly expressed in several cancer tissues or testicular tissues. Our previous study had revealed that elevated BAP31 plays a crucial role in the progress and metastasis of cervical cancer. Even so, the precise mechanism of abnormal BAP31 elevation in cervical cancer has not been fully elucidated. We revealed that the expression of BAP31 was mainly regulated by microRNA‐362 (miR‐362), which was markedly downregulated in cervical cancer tissues and negatively correlated with clinical tumor staging. Overexpression of miR‐362 inhibited cervical cancer cell proliferation and increased the proportion of apoptotic cells. Furthermore, miR‐362 reduced the tumor sizes and prolonged mice survival time in xenograft nude mice model. Finally, we demonstrated that the BAP31/SPTBN1 complex regulated tumor progression through the Smad 2/3 pathway under the control of miR‐362. Collectively, our findings demonstrated that miR‐362 could work as an anti‐oncomiR that inhibits proliferation and promotes apoptosis in cervical cancer cells via BAP31 and TGFβ/Smad pathway. Overexpression of miR‐362 might be a potential therapeutic strategy for cervical cancer.

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MicroRNA 362-3p Reduces hERG-related Current and Inhibits Breast Cancer Cells Proliferation

Cited by 27 publications

References 38 publications

miR-362-3p acts as a tumor suppressor by targeting SERBP1 in ovarian cancer

miR-362-3p acts as a tumor suppressor by targeting SERBP1 in ovarian cancer

The molecular mechanisms of the long noncoding RNA SBF2-AS1 in regulating the proliferation of oesophageal squamous cell carcinoma

MiR‐362 suppresses cervical cancer progression via directly targeting BAP31 and activating TGFβ/Smad pathway

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