Twist induces epithelial-mesenchymal transition in cervical carcinogenesis by regulating the TGF-β/Smad3 signaling pathway

Fan, Qiong; Qiu, Mei Ting; Zhu, Zhu; Zhou, Jin; Chen, Limo; Zhou, Ye; Gu, Wei; Wang, Li Hua; Li, Zhu Nan; Xu, Ying; Cheng, Wei; Wu, Dan; Bao, Wei

doi:10.3892/or.2015.4143

Cited by 54 publications

(41 citation statements)

References 38 publications

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“…Recent studies have shown that activation of TGFA/Smad3 signal can induce the migration and invasion of cervical cancer cell lines, suggesting that it plays a vital role in cervical cancer metastasis. 32 These results are consistent with our findings that miR-195 level negatively correlates with advanced clinical stage and lymphatic metastasis of cervical cancer and that Smad3 is a functional target of miR-195. We showed that overexpression of Smad3 abrogated tumor suppressive effects of miR-195 on cervical cancer cell migration and invasion.…”

Section: Discussionsupporting

confidence: 94%

MiR-195 Suppresses Cervical Cancer Migration and Invasion Through Targeting Smad3

Zhou¹,

Han²,

Zhou³

et al. 2016

Int J Gynecol Cancer

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Section: Discussionsupporting

confidence: 94%

MiR-195 Suppresses Cervical Cancer Migration and Invasion Through Targeting Smad3

Zhou¹,

Han²,

Zhou³

et al. 2016

Int J Gynecol Cancer

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“…Consistent with the results of Meng et al ., we observed that the knockdown of PODXL expression inhibited TGF‐β‐induced EMT of A549 cells (data not shown). Although many transcript factors, including Snail and Twist, are known to regulate EMT, immunoblotting did not reveal upregulation of Snail or Twist in PODXL‐OE cells. However, EMT was induced by PODXL expression, as shown by changes in EMT markers, including E‐cadherin, N‐cadherin, vimentin, fibronectin and αSMA.…”

Section: Discussionsupporting

confidence: 92%

Podocalyxin influences malignant potential by controlling epithelial–mesenchymal transition in lung adenocarcinoma

et al. 2017

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Epithelial–mesenchymal transition (EMT) plays an important role in the progression of lung carcinoma. Podocalyxin (PODXL), which belongs to the CD34 family and regulates cell morphology, has been linked to EMT in lung cancer, and PODXL overexpression is associated with poor prognosis in several different classes of cancers. The aim of this study was to clarify the role of PODXL overexpression in EMT in lung cancer, and to determine the prognostic value of PODXL overexpression in tumors from lung cancer patients. The morphology, EMT marker expression, and migration and invasion abilities of engineered A549 PODXL‐knockdown (KD) or PODXL‐overexpression (OE) lung adenocarcinoma cells were examined. PODXL expression levels were assessed by immunohistochemistry in 114 human clinical lung adenocarcinoma specimens and correlated with clinical outcomes. PODXL‐KD cells were epithelial in shape, whereas PODXL‐OE cells displayed mesenchymal morphology. Epithelial markers were upregulated in PODXL‐KD cells and downregulated in PODXL‐OE cells, whereas mesenchymal markers were downregulated in the former and upregulated in the latter. A highly selective inhibitor of phosphatidylinositol 3‐kinase‐Akt signaling attenuated EMT of PODXL‐OE cells, while a transforming growth factor inhibitor did not, suggesting that PODXL induces EMT of lung adenocarcinoma cells via the phosphatidylinositol 3‐kinase pathway. In lung adenocarcinoma clinical specimens, PODXL expression was detected in minimally invasive and invasive adenocarcinoma, but not in non‐invasive adenocarcinoma. Disease free survival and cancer‐specific survival were significantly worse for patients whose tumors overexpressed PODXL. PODXL overexpression induces EMT in lung adenocarcinoma and contributes to tumor progression.

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“…Cervical cancers can be further classified to the well, moderately and poorly differentiated subtypes (Yoo et al, ). The poorly differentiated CCs usually grow more aggressively and lead high metastatic rates because of their strong EMT tendency (Miao et al, ; Fan et al, ). We therefore analyzed the relevance of S100A4 upregulation and membrane E‐cadherin reduction with the grades of CCs.…”

Section: Discussionmentioning

confidence: 99%

Inversed Expression Patterns of S100A4 and E‐Cadherin in Cervical Cancers: Implication in Epithelial–Mesenchymal Transition

Liu

Yang

et al. 2017

The Anatomical Record

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Cervical cancer/CC is the third commonest female malignancy worldwide. The aggressive growth and distal metastases are the leading causes of CC mortality, which is largely due to epithelial-mesenchymal transition/EMT. Fibroblast specific protein S100A4 promotes cancer metastasis and epithelial type cadherin/E-cadherin play pivotal roles in cell-cell and cell-extracellular matrix interaction. Therefore, the expression patterns of S100A4 and E-cadherin reflect statuses of EMT of carcinoma cells. However, S100A4 expression and its relevance with E-cadherin and HPV16 infection in cervical cancers remain unknown. This study aims to address the above issues using cervical cancer specimens. Immunohistochemistry reveals that the levels of mesenchymal marker S100A4 is upregulated (>++) in cervical adenocarcinomas/CACs (12/16; 75%) and squamous cell carcinomas/CSCCs (23/28; 82%) than that in noncancerous glandular epithelia/GE (0/12; 0%) and squamous epithelia/SE (0/12; 0%). Epithelial marker membranous E-cadherin is remarkably reduced on the surface of CAC and CSCC cells (P = 0.00; P = 0.00), especially those showing poorly differentiated phenotypes (P < 0.05) in comparison with their noncancerous counterparts. Correlative analyses revealed an inverse relationship between S100A4 and E-cadherin expression among the cervical cancer samples (P = 0.01, r = -0.38). S100A4 expression level in HPV16-infected group is higher than that in HPV16-free group (P = 0.02). These results suggest the close correlation of S100A4 upregulation with cervical cancer formation and HPV16 infection and E-cadherin reduction with the grades of CC dedifferentiation. The concurrent gain of S100A4 and loss of membrane E-cadherin suggest EMT tendency of CC cells and can be regarded as an unfavorable prognostic parameter of CC patients. Anat Rec, 300:2184-2191, 2017. © 2017 Wiley Periodicals, Inc.

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Twist induces epithelial-mesenchymal transition in cervical carcinogenesis by regulating the TGF-β/Smad3 signaling pathway

Cited by 54 publications

References 38 publications

MiR-195 Suppresses Cervical Cancer Migration and Invasion Through Targeting Smad3

MiR-195 Suppresses Cervical Cancer Migration and Invasion Through Targeting Smad3

Podocalyxin influences malignant potential by controlling epithelial–mesenchymal transition in lung adenocarcinoma

Inversed Expression Patterns of S100A4 and E‐Cadherin in Cervical Cancers: Implication in Epithelial–Mesenchymal Transition

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