miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

Chang, Yongmei; Yan, Wensen; Sun, Cong; Li, Qingfeng; Wang, Jun

doi:10.3892/ol.2017.7092

Cited by 29 publications

(40 citation statements)

References 38 publications

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“…Similar to our study, recent studies have shown that MAP3K1 is functionally required for multiple physiological processes, including cell growth, cell migration, and apoptosis, and is strongly correlated with poor outcomes in a wide range of malignant cancers. [13][14][15] Furthermore,…”

Section: Discussionmentioning

confidence: 99%

“…another study demonstrated that MAP3K1 promotes tumorigenesis in nonsmall cell lung cancer cells by regulating epithelial-mesenchymal transition through miR-145-5p-mediated JNK signaling pathway activation, suggesting the potential role of MAP3K1 as an important oncogene. 12,15,35 Increasing evidence has indicated that acquired resistance to chemotherapy and radiation leads to the rapid recurrence and poor prognosis of glioma in patients. 36 According to our results, MAP3K1…”

Section: Discussionmentioning

confidence: 99%

“…The activation of MAPK networks includes 3 sequential phosphorylation strategies, from MAPK kinase kinases (MAP3Ks) to MAPK kinase (MAP2Ks) and MAPKs . Mitogen‐activated protein kinase kinase kinase 1 (MAP3K1), which is an important isoform for the first stimulation step of MAPKs, participates in regulating physiological and pathological processes, such as cell growth, cell migration, and apoptosis in gastric cancer, breast cancer, and nonsmall cell lung cancer cells . Additionally, a mechanistic study has indicated that MAP3K1 promotes tumor progression via the specific phosphorylation of MAP2K4 and thus selectively phosphorylates and activates c‐Jun N‐terminal kinase (JNK) .…”

Section: Introductionmentioning

confidence: 99%

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Combined elevation of TRIB2 and MAP3K1 indicates poor prognosis and chemoresistance to temozolomide in glioblastoma

et al. 2019

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Introduction Glioblastoma (GBM) is the most lethal primary malignant brain tumor in adults with poor survival due to acquired therapeutic resistance and rapid recurrence. Currently, the standard clinical strategy for glioma includes maximum surgical resection, radiotherapy, and temozolomide (TMZ) chemotherapy; however, the median survival of patients with GBM remains poor despite these comprehensive therapies. Therefore, the identification of new prognostic biomarkers is urgently needed to evaluate the malignancy and long‐term outcome of glioma. Aims To further investigate prognostic biomarkers and potential therapeutic targets for GBM. Results In this study, we identified tribbles pseudokinase 2 (TRIB2) as one of the genes that is most correlated with pathological classification, radioresistance, and TMZ resistance in glioma. Additionally, the expression of mitogen‐activated protein kinase kinase kinase 1 (MAP3K1) showed a strong correlation with TRIB2. Moreover, a combined increase in TRIB2 and MAP3K1 was observed in GBM and indicated a poor prognosis of patients with glioma. Finally, enriched TRIB2 expression and MAP3K1 expression were shown to be associated with resistance to TMZ and radiotherapy. Conclusion Combined elevation of TRIB2 and MAP3K1 could be novel prognostic biomarkers and potential therapeutic targets to evaluate the malignancy and long‐term outcomes of GBM.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Combined elevation of TRIB2 and MAP3K1 indicates poor prognosis and chemoresistance to temozolomide in glioblastoma

et al. 2019

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“…Western blotting analysis was performed as described previously [4]. Cell lysates were prepared with RIPA buffer containing protease and phosphatase inhibitor cocktail on ice then then concentrations of protein were measured by using the Bradford method.…”

Section: Western Blottingmentioning

confidence: 99%

“…to either chemotherapeutics or radiation, which leads to more frequent recurrence compared to low grade glioma [3]. A wide range of molecular pathways and regulation factors have been proved to be required for GBM growth and therapy resistance, which might be potential therapeutic targets for GBM treatment [4]. Therefore, it is meaningful for researchers to deeply investigate the mechanism included in the biological behaviors of GBM.…”

mentioning

confidence: 99%

Nuclear Factor I A Promotes Temozolomide Resistance in Glioblastoma via Transcriptional Regulation of Nuclear Factor κB Pathway

Wang

Zuo

et al. 2019

Preprint

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Background: Glioma is one of the most common primary brain tumors in human with severe mortality based on its therapy resistance and recurrence. Many molecular pathways and regulation factors have been proved to be required for GBM growth and therapy resistance, however, the underlying molecular mechanisms still remains unclear. Methods: Nuclear factor I-A (NFIA) was identified as a key candidate kinase encoding gene in chemoresistance regulation by using kinome-wide bioinformatic analysis. Afterwards, the potential biological functions of NFIA in oncogenesis and chemoresistance were clarified by qRT-PCR, western blotting and in vivo xenograft models followed by temozolomide (TMZ) resistant U87 cell induction. Additionally, immunohistochemistry (IHC) assays were performed to explore the clinical significance of AURKB in glioma patients. At last, lentiviral silencing of NFIA was used to explore the potential downstream targets for NFIA in acquired TMZ resistance in GBM.. Results: We identified NFIA was the most correlated gene for TMZ resistance in GBM. Clinically, elevated NFIA expression was significantly correlated to adverse outcomes of glioma patients especially in GBM patients. Moreover, NFIA was functionally required for TMZ resistance of U87 cells while suppression of NFIA via lentivirus infection reduced cell proliferation, tumorigenesis as well as resistance to TMZ in GBM cells. Lastly, NFIA promoted acquired TMZ resistance in GBM via transcription activity thus regulated the expression of nuclear factor κB (NF-kB). Conclusions: Altogether, our study suggests that NFIA-dependent transcriptional regulation of NF-kB contributes to the acquired TMZ resistance in GBM, indicating that NFIA-NF-κB axis could be a new therapeutic target for TMZ resistant GBM.

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Retracted: miR‐145 modulates epithelial‐mesenchymal transition and invasion by targeting ZEB2 in non–small cell lung cancer cell lines

Li¹,

Chen

Wang

et al. 2018

J of Cellular Biochemistry

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Lung cancer is the leading cause of cancer‐related deaths worldwide. Epithelial‐mesenchymal transition (EMT) is a major event that drives cancer progression. Here we aim to investigate the role of microRNA, miR‐145, in regulating EMT of the highly invasive non–small cell lung cancer (NSCLC). Quantitative real‐time polymerase chain reaction analysis indicated that miR‐145 was downregulated in cancer tissue compared with that in adjacent normal tissue. NSCLC cell lines, namely H1299, PC7, and SPCA‐1, also demonstrated miR‐145 downregulation, which is correlated well with their invasive ability, assessed by the Matrigel invasion assay. miR‐145 overexpression resulted in downregulation of N‐cadherin, and downregulation of vimentin and E‐cadherin, suggesting a decreased EMT activity. TargetScan analysis predicted that a binding site exists between miR‐145 and an oncogene, ZEB2, which was verified using the dual‐luciferase assay. Alteration of miR‐145 expression also induced inverse effects on ZEB2 expression, and a negative correlation exists between ZEB2 and miR‐145 in human tissues. ZEB2 and miR‐145 also exerted antagonizing effects on the invasion of NSCLC cells. Therefore, miR‐145 is an important molecule in NSCLC that regulates cancer EMT through targeting ZEB2.

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miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

Cited by 29 publications

References 38 publications

Combined elevation of TRIB2 and MAP3K1 indicates poor prognosis and chemoresistance to temozolomide in glioblastoma

Combined elevation of TRIB2 and MAP3K1 indicates poor prognosis and chemoresistance to temozolomide in glioblastoma

Nuclear Factor I A Promotes Temozolomide Resistance in Glioblastoma via Transcriptional Regulation of Nuclear Factor κB Pathway

Retracted: miR‐145 modulates epithelial‐mesenchymal transition and invasion by targeting ZEB2 in non–small cell lung cancer cell lines

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