MicroRNA-134-3p inhibits ovarian cancer progression by targeting flap structure-specific endonuclease 1 in vitro

Zhao, Mei; Ji, Hongjie; Fu, Qiang; Qian, Cheng; Zhang, Yu; Yang, Yu

doi:10.3892/or.2020.7844

Cited by 10 publications

(14 citation statements)

References 24 publications

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“…Many miRNAs have been determined to be involved in the development of ovarian cancer. MiR-134-3p inhibited the progression of ovarian cancer via targeting flap structure-specific endonuclease 1 in vitro (Zhao et al 2020 ). MiR-195 regulated tumor growth and MICU1 expression in ovarian.…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG20 promotes cell proliferation and invasion by suppressing miR-217 in ovarian cancer

Xing

Chen

2021

Genes Genom

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Background Ovarian cancer is the most common female gynecological malignancy. SNHG20, as a long non-coding RNA, has been proven to be an important regulator in the occurrence and development of various tumors. However, the potential mechanism of SNHG20 in ovarian cancer is unclear. Objective The present study was aimed to investigate the functions and mechanisms of SNHG20 in ovarian cancer. Methods The expression of SNHG20 and miR-217 in ovarian cancer tissues and cell lines was detected by qRT-PCR. CCK-8 assay was used to measure cell proliferation in transfected cells. The transwell assay was used to detect the relative invasion rate of transfected cells. The putative binding sites between SNHG20 and miR-217 were predicted by software LncBase v.2, and the interaction between SNHG20 and miR-217 was confirmed by dual-luciferase reporter assays and RIP assay. The rescue experiments were used to illustrate potential mechanisms. Results SNHG20 was upregulated in ovarian cancer tissues and cell lines. Overexpression of SNHG20 promoted ovarian cancer cell proliferation and invasion. MiR-217 was downregulated in ovarian cancer tissues and cells, and was negatively regulated by SNHG20. Moreover, miR-217 overexpression inhibited ovarian cancer cell proliferation and invasion. Furthermore, miR-217 mimic reversed the inhibitory effect of SNHG20 overexpression on the biological behavior of ovarian cancer cells. Conclusions SNHG20 promoted cell proliferation and invasion by sponging miR-217 in ovarian cancer. These results suggested that SNHG20 and miR-217 might provide new targets for therapeutic application in ovarian cancer.

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Section: Discussionmentioning

confidence: 99%

LncRNA SNHG20 promotes cell proliferation and invasion by suppressing miR-217 in ovarian cancer

Xing

Chen

2021

Genes Genom

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“…Interestingly, miR-134-3p has been described by others to inhibit cancer progression. For example, in ovarian cancer it was demonstrated that miR-134-3p overexpression lowered ovarian cancer cell proliferation and caused cell cycle arrest as well as migration and invasion [36]. With respect to ovarian cancer, the effects were partially caused by down-regulated expression of FEN1 mediated by miR-134-3p [36].…”

Section: Discussionmentioning

confidence: 99%

“…For example, in ovarian cancer it was demonstrated that miR-134-3p overexpression lowered ovarian cancer cell proliferation and caused cell cycle arrest as well as migration and invasion [36]. With respect to ovarian cancer, the effects were partially caused by down-regulated expression of FEN1 mediated by miR-134-3p [36]. Also, for small-cell lung cancer, a tumor-suppressive function of miR-134 was shown.…”

Section: Discussionmentioning

confidence: 99%

SOX9 is a Target of miR-134-3p And miR-224-3p in Beast Cancer Cell Lines

Chao

Kordaß

Osen

et al. 2021

Preprint

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SOX9 represents a transcription factor identified as an important mediator of cancer progression in breast cancer. miRNAs are small non-coding RNAs that can inhibit translation of target genes by binding to the 3’-UTR region of the respective mRNA molecule. Deregulated miRNA expression plays a pivotal role in hallmarks of cancer such as sustained proliferation and inhibition of apoptosis. In this study we investigated the miRNA-mediated regulation of SOX9 expression in two breast cancer cell lines providing further insights into cellular mechanisms driving breast cancer progression. The effect of miR-134-3p, miR-224-3p and miR-6859-3p on SOX9 expression was tested on mRNA as well as protein level in the human breast cancer cell line MDA-MB-231. Furthermore, direct binding of these miRNAs to the SOX9 3’-UTR was assessed by luciferase reporter assays and site-directed mutagenesis in MDA-MB-231 and MCF-7 cells. SOX9 expression was significantly reduced on mRNA and protein level by transfection of either miR-134-3p, miR-224-3p or miR-6859-3p. Luciferase reporter assays proved direct binding of miR-134-3p and miR-224-3p to the SOX9 3’-UTR in MDA-MB-231 and MCF-7 cells. Expression analysis performed in silico revealed reduced expression of both miRNAs in breast cancer tissues. We describe three novel miRNAs capable of targeting SOX9 in human breast cancer cell lines. For miR-134-3p and miR-224-3p direct interaction with the SOX9 3’-UTR was proven. Furthermore, miR-134-3p and miR-224-3p reduced breast cancer cell viability, which is in line with the tumorigenic effects reported for SOX9 in breast cancer.

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“…This has been observed in cervical cancer, breast cancer, and non-small cell lung cancer (NSCLC) [ 11 – 13 ]. A study revealed that miR-134-3p, a FEN1 inhibitor, considerably decreased cell proliferation, migration, and invasion and increased apoptosis in human ovarian cancer [ 14 ]. However, the function of miR-4324 and FEN1 in ovarian cancer remains unclear.…”

Section: Introductionmentioning

confidence: 99%

miR-4324 inhibits ovarian cancer progression by targeting FEN1

You-liang

Yuan

et al. 2022

J Ovarian Res

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Background Ovarian cancer is one of the most lethal malignancies, with a 1.9% mortality rate worldwide. The dysregulation of the FEN1 gene and miR-4324 has been associated with cancer progression. However, the relationship between miR-4324 and-FEN1 requires further investigation. Methods miR-4324 and FEN1 expressions in ovarian cancer tissues and cell lines were measured via RT-qPCR. The interaction between miR-4324 and FEN1 was assessed using luciferase and RNA pull-down assays. The effects of miR-4324 and FEN1 on cell proliferation, adhesion and apoptosis were determined by CCK-8, BrdU, colony formation, cell adhesion, Caspase-3 and western blot assays in ovarian cancer cell lines CaOV3 and OVCAR3, respectively. Results The results showed that miR-4324 expression was significantly decreased and FEN1 expression was enhanced in ovarian cancer tissues and cell lines. miR-4324 inhibitor promoted cell proliferation, adhesion and migration, and prevented apoptosis. Furthermore, the downregulation of FEN1 inhibited ovarian cancer cell growth and increased apoptosis. miR-4324 inhibited FEN1 expression and repressed ovarian cancer progression. Conclusion Our study found that miR-4324 inhibited FEN1 expression, suppressed cell growth, and increased apoptosis in ovarian cancer cells. Therefore, we identified miR-4324 and FEN1 as potential therapeutic targets for ovarian cancer treatment.

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MicroRNA-134-3p inhibits ovarian cancer progression by targeting flap structure-specific endonuclease 1 in vitro

Cited by 10 publications

References 24 publications

LncRNA SNHG20 promotes cell proliferation and invasion by suppressing miR-217 in ovarian cancer

LncRNA SNHG20 promotes cell proliferation and invasion by suppressing miR-217 in ovarian cancer

SOX9 is a Target of miR-134-3p And miR-224-3p in Beast Cancer Cell Lines

miR-4324 inhibits ovarian cancer progression by targeting FEN1

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