Protein 4.1N acts as a potential tumor suppressor linking PP1 to JNK-c-Jun pathway regulation in NSCLC

Wang, Zi; Ma, Buyun; Li, Hui; Xiao, Xiaojuan; Zhou, Weihua; Liu, Feng; Zhang, Bin; Zhu, Min; Yang, Qin; Zeng, Yayue; Sun, Yang; Sun, Shuming; Wang, Yanpeng; Zhang, Yibin; Weng, Haibo; Chen, Lixiang; Ye, Mao; An, Xiuli; Liu, Jing

doi:10.18632/oncotarget.6312

Cited by 26 publications

(29 citation statements)

References 44 publications

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“…It was previously demonstrated that protein 4.1N, a member of the protein 4.1 family, was able to suppress metastasis by inactivating JNK-c-Jun signaling pathway in NSCLC (34). Celastrol induces cisplatin re-sensitization through inhibition of the JNK/activating transcription factor 2 signaling pathway in NSCLC (35).…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2017

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Abstract. Lung cancer is one of the most common types of tumors and the leading cause of cancer-associated mortality in the world. Additionally, non-small cell lung cancer (NSCLC) accounts for ~80% of all lung cancer cases. Epithelialmesenchymal transition (EMT) is an important cell biological process, which is associated with cancer migration, metastasis, asthma and fibrosis in the lung. In the present study, it was revealed that miR-145-5p was able to suppress EMT by inactivating the c-Jun N-terminal kinase (JNK) signaling pathway in NSCLC cells. Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) was predicted and confirmed to be a novel target of miR-145-5p. Overexpression of MAP3K1 was able to reverse the inhibition of EMT induced by miR-145-5p via the JNK signaling pathway. Overall, the results revealed that miR-145-5p inhibits EMT via the JNK signaling pathway by targeting MAP3K1 in NSCLC cells.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2017

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“…Experimental protocols were conducted according to our published protocol23. Transfected cells were seeded in 6-well cell culture plates and cultured until 90–100% confluent in complete medium.…”

Section: Methodsmentioning

confidence: 99%

“…Experimental protocols were conducted according to our published protocol23. Cells (4 × 10 5 cells/well) were transfected and seeded into the top chamber of 24-well Transwell plates (Corning Incorporated, USA) containing 1% FBS medium.…”

Section: Methodsmentioning

confidence: 99%

“…Experimental protocols were conducted according to our published protocol23. Cells or tissues were lysed with RIPA buffer (150 mM NaCl, 25 mM Tris-HCl, pH 7.4, 0.1% SDS, 1% Triton X-100, 1% deoxycholate, 2 mM EDTA) that contained a protease or phosphatase inhibitor mixture (Roche, France); 50 μg of proteins were separated by SDS-PAGE followed by immunoblotting with specific antibodies (Supplementary Table 2).…”

Section: Methodsmentioning

confidence: 99%

“…The procedure used has been described in detail in our earlier study23. Briefly, the slides were deparaffinized in xylene and dehydrated.…”

Section: Methodsmentioning

confidence: 99%

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MiR-150 promotes cellular metastasis in non-small cell lung cancer by targeting FOXO4

Ouyang

Wang

et al. 2016

Sci Rep

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Previous studies have shown that dysregulation of microRNA-150 (miR-150) is associated with aberrant proliferation of human non-small cell lung cancer (NSCLC) cells. However, whether miR-150 has a critical role in NSCLC cell metastasis is unknown. Here, we reveal that the critical pro-metastatic role of miR-150 in the regulation of epithelial-mesenchymal-transition (EMT) through down-regulation of FOXO4 in NSCLC. In vitro, miR-150 targets 3′UTR region of FOXO4 mRNA, thereby negatively regulating its expression. Clinically, the expression of miR-150 was frequently up-regulated in metastatic NSCLC cell lines and clinical specimens. Contrarily, FOXO4 was frequently down-regulated in NSCLC cell lines and clinical specimens. Functional studies show that ectopic expression of miR-150 enhanced tumor cell metastasis in vitro and in a mouse xenograft model, and triggered EMT-like changes in NSCLC cells (including E-cadherin repression, N-cadherin and Vimentin induction, and mesenchymal morphology). Correspondingly, FOXO4 knockdown exhibited pro-metastatic and molecular effects resembling the effect of miR-150 over-expression. Moreover, NF-κB/snail/YY1/RKIP circuitry regulated by FOXO4 were likely involved in miR-150-induced EMT event. Simultaneous knockdown of miR-150 and FOXO4 abolished the phenotypic and molecular effects caused by individual knockdown of miR-150. Therefore, our study provides previously unidentified pro-metastatic roles and mechanisms of miR-150 in NSCLC.

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EphA‐Mediated Regulation of Stomatin Expression in Prostate Cancer Cells

Nishida,

Sato,

Shimizu

et al. 2024

Cancer Medicine

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Background and AimsTumor growth and progression are affected by interactions between tumor cells and stromal cells within the tumor microenvironment. We previously showed that the expression of an integral membrane protein, called stomatin, was increased in cancer cells following their association with stromal cells. Additionally, stomatin impaired the Akt signaling pathway to suppress tumor growth. However, it remains unclear how stomatin expression is regulated. To explore this, we examined the cell surface molecules that can transduce the intercellular communication signals between cancer cells and stromal cells.ResultsAmong these molecules, EphA3 and EphA7 receptors and their ligand ephrin‐A5 were found to be expressed in prostate cancer cells, but not in prostate stromal cells. Cell‐to‐cell contact of prostate cancer cells through the EphA–ephrin‐A interaction suppressed stomatin expression, while knockdown of EphA3/7 or ephrin‐A5 increased stomatin expression. This increase contributed to an inhibition of prostate cancer cell proliferation. Intracellularly, the binding of ephrin‐A to EphA attenuated extracellular signaling‐regulated kinase (ERK) activation that promoted stomatin expression. Furthermore, ELK1 and ELK4, which are Ets family transcription factors phosphorylated by ERK, were involved in the induction of stomatin expression. We also found that higher Gleason score prostate cancer tissue samples had increased activation of EphA, while the stomatin expression and activated ERK and ELK levels were all low. In the mouse xenograft tumor samples generated by implantation of prostate cancer cells, EphA3 phosphorylation was attenuated and the ERK–ELK signaling and stomatin expression were enhanced in the area where stromal cells infiltrated the tumor.ConclusionThe EphA‐mediated signaling suppresses the ERK–ELK pathway, leading to the reduction of stomatin expression that affects prostate cancer malignancy.

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Protein 4.1N acts as a potential tumor suppressor linking PP1 to JNK-c-Jun pathway regulation in NSCLC

Cited by 26 publications

References 44 publications

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

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

MiR-150 promotes cellular metastasis in non-small cell lung cancer by targeting FOXO4

EphA‐Mediated Regulation of Stomatin Expression in Prostate Cancer Cells

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