Activation of STAT transcription factors by the Rho-family GTPases

Corry, Jessica; Mott, Helen R.; Owen, Darerca

doi:10.1042/bst20200468

Cited by 27 publications

(23 citation statements)

References 65 publications

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“…Interestingly, a β-Pix-CDC42 pathway has recently been identified to regulate perineural invasion in pancreatic cancer ( Chernichenko et al, 2020 ). The basis of the small increases in total CDC42 detected upon CD99 depletion are unclear, but might result from the altered activity of transcription factors and/or post-translational modifications of CDC42 that occur downstream of CDC42 activation and actin reorganisation ( Corry et al, 2020 ; Haga and Ridley, 2016 ; Hall, 2012 ; Medjkane et al, 2009 ; Perona et al, 1997 ). Importantly, the requirement for CDC42 activity in TEM and metastasis is linked to the CDC42-dependent induction of the ITGB1 gene, with β1 integrin playing a critical role in tumour cell intercalation into the endothelium ( Reymond et al, 2012 ).…”

Section: Discussionmentioning

confidence: 99%

Tumour cell CD99 regulates transendothelial migration via CDC42 and actin remodelling

Mannion

Odell

Taylor

et al. 2021

Journal of Cell Science

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Metastasis requires tumour cells to cross endothelial cell (EC) barriers using pathways similar to those used by leucocytes during inflammation. Cell surface CD99 is expressed by healthy leucocytes and EC and participates in inflammatory transendothelial migration (TEM). Tumour cells also express CD99 and we have analysed its role in tumour progression and cancer cell TEM. Tumour cell CD99 was required for adhesion to ECs, but inhibited invasion of the endothelial barrier and migratory activity. Furthermore, CD99 depletion in tumour cells caused redistribution of the actin cytoskeleton and increased activity of the Rho GTPase CDC42, known for its role in actin remodelling and cell migration. In a xenograft model of breast cancer, tumour cell CD99 expression inhibited metastatic progression and patient samples showed reduced expression of the CD99 gene in brain metastases compared to matched primary breast tumours. We conclude that CD99 negatively regulates CDC42 and cell migration. However, CD99 has both pro- and anti-tumour activity and our data suggests that this results in part from its functional linkage to CDC42 and the diverse signalling pathways downstream of this Rho GTPase.

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Section: Discussionmentioning

confidence: 99%

Tumour cell CD99 regulates transendothelial migration via CDC42 and actin remodelling

Mannion

Odell

Taylor

et al. 2021

Journal of Cell Science

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“…And the experiments confirmed that the major phosphorylation site of STAT3 by JNKs was identified to be Ser-727 in vitro ( Lim and Cao, 1999 ; Schuringa et al, 2000 ; Miyazaki et al, 2008 ). The STAT family of transcription factors integrated cytokine and growth factor signaling to transcriptionally regulate a diverse array of cellular processes ( Corry et al, 2020 ). STAT3 had become one of the common investigated oncogenic transcription factors and was associated with cell proliferation, differentiation, progression, metastasis and chemoresistance ( Qin et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

The Prognostic Significance of Anisomycin-Activated Phospho-c-Jun NH2-Terminal Kinase (p-JNK) in Predicting Breast Cancer Patients’ Survival Time

Chen

Kong

et al. 2021

Front. Cell Dev. Biol.

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This study aims to investigate the prognostic significance of p-JNK in breast cancer patients receiving neoadjuvant chemotherapy (NACT) and analyze the relationship between anisomycin, p-JNK. A total of 104 breast cancer patients had NACT were enrolled in this study. The western blot and immunohistochemistry assays were used to determine the protein expressions of p-JNK in human breast cancer cell lines and patients’ cancer tissues. The chi-square test and Fisher’s exact test were adopted to gauge the associations between breast cancer and clinicopathological variables by p-JNK expression, whereas the univariate and multivariate Cox proportional hazards regression models were used to analyze the prognostic value of p-JNK expression. The Kaplan-Meier plots and the log-rank test were adopted to determine patients’ disease-free survival (DFS) and overall survival (OS). Findings indicated that the p-JNK expression had prognostic significance in univariate and multivariate Cox regression survival analyses. Results of log-rank methods showed that: (1) the mean DFS and OS times in patients with high p-JNK expression were significantly longer than those in patients with low p-JNK expression (χ2 = 5.908, P = 0.015 and χ2 = 6.593, P = 0.010, respectively). p-JNK expression is a significant prognostic factor that can effectively predict the survival in breast cancer patients receiving NACT. Treatment with the JNK agonist anisomycin can induce apoptosis, lead to increased p-JNK expression and decreased p-STAT3 expression. Moreover, the p-JNK expression was inversely correlated with p-STAT3 expression.

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“…The Rho-family control pathways involved in cellular morphology, which are commonly activated in cancer cell invasion and metastasis [ 22 ]. And Rho guanosine triphosphatases (GTPases) have well-recognized roles in regulating various downstream signaling pathways in a wide range of cancers [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

FAM65A as a novel prognostic biomarker in human tumors reveal by a pan-cancer analysis

Liang

Wei

et al. 2021

Discov Onc

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Background Family with sequence similarity 65 member A (FAM65A), also known as RIPOR1, is differentially expressed between human tumor and non-tumor tissues in kinds of cancers. In addition, it was reported that the product of FAM65A may be a biomarker for cholangiocarcinoma patients. However, there is still no evidence on the relationship between the FAM65A and different types of tumors. Our study is mainly for exploring the prognostic values of FAM65A in pan-cancer and for further discovering a potential therapeutics target. Methods We analyzed FAM65A expression, prognostic values, genetic alteration, protein phosphorylation, immune infiltration and enrichment analysis across different types of human malignant tumors based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. Additionally, Real-Time PCR (RT-qPCR) was performed to further confirm the roles of FAM65A in the pathogenesis of colorectal cancer. Results We found that FAM65A expression was associated with the prognosis of multiple human tumors, especially colorectal cancer. Moreover, we also observed that FAM65A was highly expressed in colorectal cancer through RT-qPCR. We observed that decreasing phosphorylation level of the S351 locus in colon adenocarcinoma, uterine corpus endometrial carcinoma and lung adenocarcinoma. And the expression of FAM65A was positively related to cancer-associated fibroblasts (CAFs) infiltration in many tumors, such as colon adenocarcinoma. Therefore, FAM65A may be a potential prognostic biomarker of human tumors.

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Activation of STAT transcription factors by the Rho-family GTPases

Cited by 27 publications

References 65 publications

Tumour cell CD99 regulates transendothelial migration via CDC42 and actin remodelling

Tumour cell CD99 regulates transendothelial migration via CDC42 and actin remodelling

The Prognostic Significance of Anisomycin-Activated Phospho-c-Jun NH2-Terminal Kinase (p-JNK) in Predicting Breast Cancer Patients’ Survival Time

FAM65A as a novel prognostic biomarker in human tumors reveal by a pan-cancer analysis

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