A new PKCα/β/TBX3/E-cadherin pathway is involved in PLCε-regulated invasion and migration in human bladder cancer cells

Du, Hong; Ou, Li Ping; Yang, Xue; Song, Xue Dong; Fan, Yan; Tan, Bing; Luo, Chun; Wu, Xiao Hou

doi:10.1016/j.cellsig.2013.11.015

Cited by 39 publications

(33 citation statements)

References 39 publications

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“…Finally, as mentioned previously, they showed that TBX3 mediated the pro-migratory effect of PMA in MCF7 breast cancer cells. The regulation of TBX3 by the PKC pathway has been further supported by Du et al who showed that knocking down Phospholipase C epsilon (PLCε) in bladder cancer cell lines resulted in a corresponding inhibition of PKCα/β, which in turn reduced TBX3 mRNA and protein levels (72). Importantly, they also demonstrated that in bladder cancer the repression of E-cadherin by PKCα/β signalling is mediated by TBX3.…”

Section: Protein Kinase C (Pkc) Signalling Pathwaymentioning

confidence: 50%

“…Elevated levels of TBX3 were also shown to correlate with decreased E-cadherin levels in squamous carcinoma cells (71). In addition, work by Du et al revealed that a PKC/TBX3/E-cadherin signalling cascade exists in human bladder cancer cells and that the regulation of E-cadherin by TBX3 occurs in a PKC-dependent manner (72). It is noteworthy that in sarcomas, the ability of TBX3 to promote migration was not due to E-cadherin repression.…”

Section: Tbx3 In Tumour Formation Invasion and Metastasismentioning

confidence: 91%

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The T-Box transcription factor 3 in development and cancer

Willmer

Cooper

Peres

et al. 2017

BST

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Section: Protein Kinase C (Pkc) Signalling Pathwaymentioning

confidence: 50%

Section: Tbx3 In Tumour Formation Invasion and Metastasismentioning

confidence: 91%

The T-Box transcription factor 3 in development and cancer

Willmer

Cooper

Peres

et al. 2017

BST

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“…Therefore, calphostin C mainly inhibited PKCα, βI, βII and γ. In addition, GO6976 had previously been demonstrated to inhibit PKC isoenzymes α and βI (21)(22)(23). In Fig.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of PKCα reduces the ability of migration of kidney cancer cells but has no impact on cell apoptosis

Zhan

Kong

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Kidney cancer is among the most important causes of cancer-associated mortality worldwide. The present study aimed to evaluate protein kinase C α (PKCα) expression in kidney cancer tissues and cell lines, and its significance in apoptosis and migration. Expression of PKCα was analyzed using quantitative polymerase chain reaction and western blotting. In addition, the inhibitor of PKCα (calphostin C and GO6976) was used to treat kidney cancer cells. The ACHN cell line was generated with PKCα-small-interfering RNA (siRNA) and a stable expression of PKCα, in order to facilitate the analysis of apoptosis and migration of PKCα during knockdown and inactivation. Flow cytometry was used to determine the rates of apoptosis. Immunohistochemical staining was used to identify the localization of PKCα in renal clear cell carcinoma and normal sections. PKCα expression in normal tissues was found to be greater than in cancerous tissues. Furthermore, apoptosis was not promoted with PKCα inhibitors or PKCα-siRNA treatment, and a decrease of the migration ability was observed following transfection with PKCα-dominant negative. The results indicated that inhibition of PKCα might not contribute to apoptosis progression in kidney carcinoma.

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“…A mutation of Tbx3 was demonstrated to be closely associated with the pluripotency of embryonic stem cells and the invasiveness of cancer (6). In resectable pancreatic carcinoma (7), melanoma (8), bladder cancer (9) and colorectal cancer (10), Tbx3 was revealed to be overexpressed and associated with poor prognosis of cancer. Recently, Tbx3 was reported to serve a key role in melanoma migration and invasion by acting as a key substrate of protein kinase B and thus inducing the repression of E-cadherin (8).…”

Section: Introductionmentioning

confidence: 99%

T-box 3 overexpression is associated with poor prognosis of non-small cell lung cancer

Jiang

Zhang

2017

Oncology Letters

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Abstract. T-box 3 (Tbx3), a member of the T-box transcription factor family, serves a crucial role in embryonic development and cancer progression. Previous studies have demonstrated the clinical significance of Tbx3 in numerous types of cancer. However, the expression level and pathological function of Tbx3 in non-small cell lung cancer (NSCLC) are unknown. To the best of our knowledge, the present study provided the first evidence demonstrating the clinicopathological significance of Tbx3 in NSCLC. Tbx3 was revealed to be overexpressed in NSCLC cell lines and tissues obtained from patients with NSCLC by reverse transcription-quantitative polymerase chain reaction and western blot analysis. Downregulation of Tbx3 by Tbx3-specific short hairpin RNA decreased cell proliferation in NSCLC cell lines, but there was a slight increase in the cell population of the G 1 phase. Furthermore, depletion of Tbx3 expression significantly decreased the cell migration distance. In addition, overexpression of Tbx3 was notably associated with tumor size, tobacco smoking status, tumor-node-metastasis stage and differentiation. These results demonstrated the importance of Tbx3 in the pathological progression of NSCLC and may serve as a potential therapeutic target for NSCLC.

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A new PKCα/β/TBX3/E-cadherin pathway is involved in PLCε-regulated invasion and migration in human bladder cancer cells

Cited by 39 publications

References 39 publications

The T-Box transcription factor 3 in development and cancer

The T-Box transcription factor 3 in development and cancer

Inhibition of PKCα reduces the ability of migration of kidney cancer cells but has no impact on cell apoptosis

T-box 3 overexpression is associated with poor prognosis of non-small cell lung cancer

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