MicroRNA-148b enhances proliferation and apoptosis in human renal cancer cells via directly targeting MAP3K9

Nie, Fang; Liu, Tianming; Liu, Zhong; Yang, Xianggui; Yun-hong, Liu; Xiao, Hong‐Wei; Liu, Xiaoqiang; Wang, Xiaoyan; Liu, Zhicheng; Zhou, Li; Mao, Zhizhong; Zhou, Qin; Chen, Tingmei

doi:10.3892/mmr.2015.4555

Cited by 24 publications

(17 citation statements)

References 26 publications

(28 reference statements)

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“…Knocking down miR-148b expression could enhance the phosphorylation of JNK.These results support our previous hypothesis that miR-148b exert anti-cancer activity in NSCLC by targeting MAPK/JNK pathway. In accordance with our study, Fang et al found that decreased miR-148b could enhance tumor cell proliferation and inhibit apoptosis in human renal cancer cells by targeting MAP3K9, which is a upstream activator of MAPK/JNK pathway [45]. At the same time, several studies have confirmed that miR148b works through the regulation of MAPK/JNK [46, 47].…”

Section: Discussionsupporting

confidence: 90%

MicroRNA-148b regulates tumor growth of non-small cell lung cancer through targeting MAPK/JNK pathway

et al. 2019

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Background MicroRNA-148b (miR-148b) has been detected in various types of tumors, and is generally viewed as a tumor suppressor. Our previous study found the decreased expression of miR-148b in human non small cell lung cancer (NSCLC) specimens and cell lines. However, the underlying mechanisms of miR-148b in regulating tumor progression remain unclear. Methods Firstly animal experiments were performed to verify whether miR-148b could inhibit the tumor growth. Then, the underlying mechanisms were studied by transfecting recombinant plasmids containing a miR-148b mimic or a negative control (NC) mimic (shRNA control) into NSCLC cell lines PC14/B and A549 cells. Tumor cells transfected with unpackaged lentiviral vectors was used as blank control. Cell proliferation capabilities were measured by using CCK-8 kit and colony formation assay. Cell cycle arrest was compared to clarify the mechanism underlying the tumor cell proliferation. Annexin V-FITC Apoptosis Detection kit was applied to investigate the effect of miR-148b on cell apoptosis. Furthermore, western blot analysis were performed to study the targeting pathway. Results We found that over-expression of miR148b could significantly inhibit tumor growth, while knocking down miR148b could obviously promote tumor growth. Further experiment showed that miR-148b inhibited tumor cell proliferation. Besides, over-expression of miR148b decreased the G2/M phase population of the cell cycle by preventing NSCLC cells from entering the mitotic phase and enhanced tumor cell apoptosis. Further western blot analysis indicated that miR148b could inhibit mitogen-activated protein kinase/Jun N-terminal kinase (MAPK/JNK) signaling by decreasing the expression of phosphorylated (p) JNK. Conclusions These results demonstrate that miR-148b could inhibit the tumor growth and act as tumor suppressor by inhibiting the proliferation and inducing apoptosis of NSCLC cells by blocking the MAPK/JNK pathway.

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Section: Discussionsupporting

confidence: 90%

MicroRNA-148b regulates tumor growth of non-small cell lung cancer through targeting MAPK/JNK pathway

et al. 2019

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“…Even though altered expression was found in tumors of distinct histology , miR‐148b seems to be a major regulator of breast cancer. While directly targeting key players of the integrin signaling like ITGA5, ROCK1, PI3KCA/p110α as well as NRAS, miR‐148b controls a pathway involved in tumor growth and metastasis.…”

Section: Effects Of Mir‐148/‐152 Family Members On Tumorigenesismentioning

confidence: 99%

The role of the miR‐148/‐152 family in physiology and disease

et al. 2017

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MicroRNAs (miRNAs) are endogenously encoded ∼22 nt small non-coding RNAs. They function as key players of many cellular processes by base pairing with target mRNAs and thereby impairing gene expression at the post-transcriptional level. Recent findings demonstrate a critical role of many miRNAs in immune cell differentiation and immune responses, which is also associated with the development and progression of many tumor and non-tumor diseases. Here we review the multifaceted miRNA-148/-152 family members consisting of miR-148a, miR-148b and miR-152. Next to regulation mechanisms that control the expression of this miRNA family, we will focus on (i) the role of miR-148a in regulating B and T lymphocyte function and its role in associated diseases and (ii) the importance of miR-148/-152 family members for cancer initiation, tumor growth and metastasis formation. In addition, this review aims to highlight some selected targets of the miRNA-148/-152 family members, which are involved in the biology of cancer and maintenance of epigenetic patterns. In conclusion, members of the miR-148/-152 family might represent prognostic markers and/or potential therapeutic targets for treatment of autoimmune disorders, chronic inflammatory diseases and multiple types of cancer.

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“…Many research have furnished important evidence revealing that MAP3K9 are connected with noteworthy cell biology. MAP3K9 suppresses proliferation and apoptosis in renal cancer cells by MAPK/c‐Jun N‐terminal kinase (JNK) signaling (Nie et al, ). Interference of MAP3K9 inhibits the motivation of extracellular‐signal‐regulated kinase (ERK) and p38 MAPK pathways, which further inhibits proliferation and promotes apoptosis of NP cells (Cai et al, ).…”

Section: Introductionmentioning

confidence: 99%

circ‐016910 sponges miR‐574‐5p to regulate cell physiology and milk synthesis via MAPK and PI3K/AKT–mTOR pathways in GMECs

Liu

Hou

Zhang

et al. 2019

Journal Cellular Physiology

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Incremental proofs demonstrate that miRNAs, the essential regulators of gene expression, are implicated in various biological procedures, including mammary development and milk synthesis. Here, the role of miR-574-5p in milk synthesis, apoptosis, and proliferation of goat mammary epithelial cells (GMECs) are explored without precedent, and the molecular mechanisms for the impacts are elucidated.Small RNA libraries were constructed using GMECs transfected with miR-574-5p mimics and negative control followed by sequencing via Solexa technology. Overall, 332 genes were distinguishingly expressed entre two libraries, with 74 genes upregulated and 258 genes downregulated. This approach revealed mitogenactivated protein kinase kinase kinase 9 (MAP3K9), an upstream activator of MAPK signaling, as a differentially expressed unigene. miR-574-5p targeted seed sequences of the MAP3K9 3′-untranslated region and suppressed its messenger RNA (mRNA) and protein levels, correspondingly. GMECs with miR-574-5p overexpression and MAP3K9 inhibition showed increased cell apoptosis and decreased cell proliferation resulting from sustained suppression of MAPK pathways, while MAP3K9 elevation manifested the opposite results. miR-574-5p repressed the phosphorylation of members of protein kinase B (AKT)-mammalian target of rapamycin pathway via downregulating MAP3K9 and AKT3, resulting in reducing the secretion of β-casein and triglycerides in GMECs. Finally, according to the constructed circular RNA (circRNA) libraries and bioinformatics prediction approach, we selected circ-016910 and found it acted as a sponge for miR-574-5p and blocked its relevant behaviors to undertake biological effects in GMECs. The circRNA-miRNA-mRNA network facilitates further probes on the function of miR-574-5p in mammary development and milk synthesis.This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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MicroRNA-148b enhances proliferation and apoptosis in human renal cancer cells via directly targeting MAP3K9

Cited by 24 publications

References 26 publications

MicroRNA-148b regulates tumor growth of non-small cell lung cancer through targeting MAPK/JNK pathway

MicroRNA-148b regulates tumor growth of non-small cell lung cancer through targeting MAPK/JNK pathway

The role of the miR‐148/‐152 family in physiology and disease

circ‐016910 sponges miR‐574‐5p to regulate cell physiology and milk synthesis via MAPK and PI3K/AKT–mTOR pathways in GMECs

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