MicroRNA-335 inhibits bladder cancer cell growth and migration by targeting mitogen-activated protein kinase 1

Sulforaphane (SFN), an isothiocyanate (ITCs) derived from glucosinolate that is found in cruciferous vegetables, has been reported to exert a promising anticancer effect in a substantial amount of scientific research. However, epidemical studies showed inconsistencies between cruciferous vegetable intake and bladder cancer risk. In this study, human bladder cancer T24 cells were used as in vitro model for revealing the inhibitory effect and its potential mechanism of SFN on cell growth. Here, a low dose of SFN (2.5 µM) was shown to promote cell proliferation (5.18–11.84%) and migration in T24 cells, whilst high doses of SFN (>10 µM) inhibited cell growth significantly. The induction effect of SFN on nuclear factor (erythroid-derived 2)-like 2 (Nrf2) expression at both low (2.5 µM) and high dose (10 µM) was characterized by a bell-shaped curve. Nrf2 and glutathione (GSH) might be the underlying mechanism in the effect of SFN on T24 cell growth since Nrf2 siRNA and GSH-depleting agent L-Buthionine-sulfoximine abolished the effect of SFN on cell proliferation. In summary, the inhibitory effect of SFN on bladder cancer cell growth and migration is highly dependent on Nrf2-mediated GSH depletion and following production. These findings suggested that a higher dose of SFN is required for the prevention and treatment of bladder cancer.

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Transcriptional cofactor Mask2 is required for YAP-induced cell growth and migration in bladder cancer cell

Journal of Cancer ◽

10.7150/jca.16438 ◽

2016 ◽

Vol 7 (14) ◽

pp. 2132-2138 ◽

Cited By ~ 13

Author(s):

Liang Dong ◽

Fan Lin ◽

Wanjun Wu ◽

Weiren Huang ◽

Zhiming Cai

Keyword(s):

Bladder Cancer ◽

Cell Growth ◽

Cancer Cell ◽

Bladder Cancer Cell ◽

Cell Growth And Migration ◽

And Migration

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Repression of breast cancer cell growth by proteasome inhibitorsin vitro: impact of mitogen-activated protein kinase phosphatase 1

Cancer Biology & Therapy ◽

10.1080/15384047.2015.1026465 ◽

2015 ◽

Vol 16 (5) ◽

pp. 780-789 ◽

Cited By ~ 5

Author(s):

Brijeshkumar S Patel ◽

Wai Sie Co ◽

Claudia Donat ◽

Mary Wang ◽

Wenchi Che ◽

...

Keyword(s):

Breast Cancer ◽

Protein Kinase ◽

Cell Growth ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Mitogen Activated Protein Kinase ◽

Cancer Cell Growth ◽

Breast Cancer Cell Growth ◽

Mitogen Activated Protein

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Heparin regulates colon cancer cell growth through p38 mitogen-activated protein kinase signalling

Cell Proliferation ◽

10.1111/j.1365-2184.2009.00649.x ◽

2010 ◽

Vol 43 (1) ◽

pp. 9-18 ◽

Cited By ~ 11

Author(s):

G. Chatzinikolaou ◽

D. Nikitovic ◽

A. Berdiaki ◽

A. Zafiropoulos ◽

P. Katonis ◽

...

Keyword(s):

Colon Cancer ◽

Protein Kinase ◽

Cell Growth ◽

Cancer Cell ◽

Colon Cancer Cell ◽

Mitogen Activated Protein Kinase ◽

Cancer Cell Growth ◽

Mitogen Activated Protein ◽

Protein Kinase Signalling

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Oncogenic Activation of AKT by MAPK6

10.1101/2020.09.23.309518 ◽

2020 ◽

Author(s):

Qinbo Cai ◽

Wei Wang ◽

Bingning Dong ◽

Wolong Zhou ◽

Tao Shen ◽

...

Keyword(s):

Protein Kinase ◽

Cell Growth ◽

Cancer Cell ◽

Kinase Domain ◽

Mitogen Activated Protein Kinase ◽

Breast Cancer Patients ◽

Cancer Cell Growth ◽

Growth And Survival ◽

Mitogen Activated Protein ◽

Normal Human

AbstractMitogen-activated protein kinase 6 (MAPK6) is an atypical MAPK closely related to MAPK4. We recently reported that MAPK4 can promote cancer by activating the Protein Kinase B (PKB/AKT) pathway of cell growth and survival. Here we report that MAPK6 overexpression also activates AKT to induce oncogenic outcomes, including transforming “normal” human epithelial cells into anchorage-independent growth and enhancing cancer cell growth. Knockdown of MAPK6 inhibited cancer cell growth and xenograft growth, supporting the tumor-promoting activities of endogenous MAPK6. Unlike MAPK4, which binds AKT through its kinase domain and phosphorylates AKT at T308, MAPK6 interacts with AKT through its C34 region and the unique C-terminal tail and phosphorylates AKT at S473 independent of mTORC2, the major AKT S473 kinase. MAPK6 overexpression is associated with decreased overall survival and the survival of lung adenocarcinoma, mesothelioma, uveal melanoma, and breast cancer patients. We conclude that MAPK6 can promote cancer by activating AKT and that targeting MAPK6 may be effective in human cancers.

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