MiR-505 mediates methotrexate resistance in colorectal cancer by targeting <i>RASSF8</i>

Chen, Yalin; Bian, Li; Zhang, Yingmei

doi:10.1111/jphp.12913

Cited by 17 publications

(17 citation statements)

References 19 publications

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“…Rassf8 is found both in the nucleus and cell membrane 33 . Rassf8 is related to the cell cycle, accelerates apoptosis, and restrains migration and invasion 52 . Overexpression of Rassf8 induces G0/G1 arrest, apoptosis, and downregulation of Cyclin D1 downstream of the WNT/β-catenin pathway.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-322 Regulates Self-renewal of Mouse Spermatogonial Stem Cells through Rassf8

Wang¹,

Li²,

Gong³

et al. 2019

Int. J. Biol. Sci.

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Spermatogonial stem cells (SSCs) are essential for spermatogenesis and male fertility. MicroRNAs (miRs) are key regulators of gene expression involved in self-renewal, differentiation, and apoptosis. However, the function and mechanisms of individual miR in regulating self-renewal and differentiation of SSCs remain unclear. Here, we report for the first time that miR-322 regulates self-renewal of SSCs. Functional assays revealed that miR-322 was essential for SSC self-renewal. Mechanistically, miR-322 promoted SSC self-renewal by targeting RASSF8 (ras association domain family 8). Moreover, the WNT/β-catenin signaling pathway was involved in the miR-322-mediated regulation. Furthermore, miR-322 overexpression increased GFRα1, ETV5 and PLZF expression but decreased STRA8, C-KIT and BCL6 expression. Our study provides not only a novel insight into molecular mechanisms regulating SSC self-renewal but also a basis for the diagnosis, treatment, and prevention of male infertility.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-322 Regulates Self-renewal of Mouse Spermatogonial Stem Cells through Rassf8

Wang¹,

Li²,

Gong³

et al. 2019

Int. J. Biol. Sci.

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“…In the present years, several studies have explored the role of miR-505 in the development of various cancers (Y. Chen et al, 2018;Liu et al, 2018;. The results of these studies have suggested that the overexpression of miR-505 suppressed the proliferation of many different types of tumors ( Y.…”

Section: Discussionmentioning

confidence: 99%

microRNA‐505 negatively regulates HMGB1 to suppress cell proliferation in renal cell carcinoma

Zhong

Qin

Zhou³

et al. 2019

Journal Cellular Physiology

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microRNAs have been recognized to regulate a wide range of biology of renal cell carcinoma (RCC). Although miR‐505 has been reported to play as a suppressor in several human tumors, the physiological function of miR‐505 in RCC still remain unknown. Therefore, the role of miR‐505 and relevant regulatory mechanisms were investigated in RCC in this study. Quantitative real‐time polymerase chain reaction was conducted to detect the expression of miR‐505 and high mobility group box 1 (HMGB1) in both RCC tissues and cell lines. Immunohistochemical staining was used to assess the correlation between HMGB1 expression and PCNA expression in RCC tissues. Subsequently, the effects of miR‐505 on proliferation were determined in vitro using cell counting kit‐8 proliferation assays and 5‐ethynyl‐2′‐deoxyuridine incorporation. The molecular mechanism underlying the relevance between miR‐505 and HMGB1 was confirmed by luciferase assay. Xenograft tumor formation was used to reflect the proliferative capacity of miR‐505 in vivo experiments. Overall, a relatively lower miR‐505 and higher HMGB1 expression in RCC specimens and cell lines were found. HMGB1 was verified as a direct target of miR‐505 by luciferase assay. In vitro, overexpression of miR‐505 negatively regulates HMGB1 to suppress the proliferation in Caki‐1; meanwhile, knock‐down of miR‐505 negatively regulates HMGB1 to promote the proliferation in 769P. In addition, in vivo overexpression of miR‐505 could inhibit tumor cell proliferation in RCC by xenograft tumor formation. Therefore, miR‐505, as a tumor suppressor, negatively regulated HMGB1 to suppress the proliferation in RCC, and might serve as a novel therapeutic target for RCC clinical treatment.

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“…MiRNAs participate in diverse molecular and cellular processes, such as cellular migration/invasion, cell growth, apoptosis and signal transduction. MiRNAs dysregulation is a hallmark of many cancers, including glioblastoma, and they can be classified into tumour‐suppressive miRNAs and onco‐miRNAs . For example, miRNA‐744 expression is strongly repressed in glioblastoma, causing elevated transforming growth factor 1 beta (TGFB1) and dishevelled 2 (DVL2) expression and increased tumour cell migration .…”

Section: Introductionmentioning

confidence: 99%

“…MiRNAs dysregulation is a hallmark of many cancers, including glioblastoma, and they can be classified into tumour-suppressive miRNAs and onco-miRNAs. [24][25][26][27][28] For example, miRNA-744 expression is strongly repressed in glioblastoma, causing elevated transforming growth factor 1 beta (TGFB1) and dishevelled 2 (DVL2) expression and increased tumour cell migration. [29] In contrast, up-regulation of miRNA-21 in glioblastoma is associated with suppression of phosphatase and tensin homolog (PTEN), as well as programmed cell death 4 (PDCD4) expression, causing enhancement of cell survival and inhibition of apoptosis.…”

Section: Introductionmentioning

confidence: 99%

MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

Alamdari-Palangi

Amini

Karami

2020

Journal of Pharmacy and Pharmacology

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Objectives Down‐regulation of miRNA‐7 is correlated with over‐expression of IRS‐1 and IRS‐2 proteins, the upstream regulators of IGF‐1R/Akt pathway, in glioblastoma cells. In this study, the effect of miRNA‐7 on expression of IRS‐1 and IRS‐2 and sensitivity of the U373‐MG glioblastoma cells to erlotinib was explored. Methods After miRNA‐7 transfection, the expression of IRS‐1 and IRS‐2 mRNAs was measured by RT‐qPCR. Trypan blue assay was used to assess the effect of miRNA‐7 on cell proliferation. The effects of miRNA‐7 and erlotinib, alone and in combination, on cell survival and apoptosis were measured using MTT assay and ELISA cell death assay, respectively. Key findings Our data showed that miRNA‐7 markedly inhibited the expression of IRS‐1 and IRS‐2 in a time‐dependent manner, inhibited the proliferation of glioblastoma cells and enhanced apoptosis (P < 0.05, relative to control). Pretreatment with miRNA‐7 synergistically inhibited the cell survival rate and decreased the IC50 of erlotinib. Furthermore, miRNA‐7 significantly augmented the apoptotic effect of erlotinib. Conclusions Our data propose that inhibition of IRS‐1 and IRS‐2 by miRNA‐7 can effectively induce apoptosis and sensitize glioblastoma cell to EGFR‐TKIs. Therefore, miRNA‐7 may be a potential therapeutic target in patients with glioblastoma.

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MiR-505 mediates methotrexate resistance in colorectal cancer by targeting RASSF8

Abstract: MiR-505 mediated MTX resistance, propagation, cell cycle and metastasis by targeting RASSF8 in colorectal cancer.

Cited by 17 publications

References 19 publications

MicroRNA-322 Regulates Self-renewal of Mouse Spermatogonial Stem Cells through Rassf8

MicroRNA-322 Regulates Self-renewal of Mouse Spermatogonial Stem Cells through Rassf8

microRNA‐505 negatively regulates HMGB1 to suppress cell proliferation in renal cell carcinoma

MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

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