Long non‑coding RNA PVT1 promotes epithelial‑mesenchymal transition via the TGF‑β/Smad pathway in pancreatic cancer cells | Zendy

Xingxing Zhang | Zendy; Wen Feng | Zendy; Jin Zhang | Zendy; Lu Ge | Zendy; Youli Zhang | Zendy; Xiaomeng Jiang | Zendy; WanXin Peng | Zendy; Dawei Wang | Zendy; Aihua Gong | Zendy; Min Xu | Zendy

Open Access

Long non‑coding RNA PVT1 promotes epithelial‑mesenchymal transition via the TGF‑β/Smad pathway in pancreatic cancer cells

Author(s) -

Xingxing Zhang,

Wen Feng,

Jin Zhang,

Lu Ge,

Youli Zhang,

Xiaomeng Jiang,

WanXin Peng,

Dawei Wang,

Aihua Gong,

Min Xu

Publication year - 2018

Publication title -

oncology reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.094

H-Index - 96

eISSN - 1791-2431

pISSN - 1021-335X

DOI - 10.3892/or.2018.6462

Subject(s) - pvt1 , epithelial–mesenchymal transition , cancer research , oncogene , gene knockdown , pancreatic cancer , smad , vimentin , transforming growth factor , biology , long non coding rna , downregulation and upregulation , cancer , microbiology and biotechnology , metastasis , cell cycle , cell culture , immunology , immunohistochemistry , biochemistry , genetics , gene

Recent studies have revealed that overexpression of long non‑coding RNA (lncRNA) PVT1 is correlated with several types of cancer. However, its role in pancreatic cancer development remains to be clarified. In the present study, we found that PVT1 promoted the growth and the epithelial‑mesenchymal transition (EMT) of pancreatic cancer cells. We first determined that PVT1 was upregulated in pancreatic cancer tissues compared with adjacent normal tissues. Knockdown of PVT1 inhibited viability, adhesion, migration and invasion. Furthermore, PVT1 knockdown reduced the expression of mesenchymal markers including Snail, Slug, β‑catenin, N‑cadherin and vimentin, while it increased epithelial marker expression of E‑cadherin. Finally, knockdown of PVT1 inhibited the TGF‑β/Smad signaling, including p‑Smad2/3 and TGF‑β1 but enhanced the expression of Smad4. In contrast, overexpression of PVT1 reversed the process. These findings revealed that PVT1 acts as an oncogene in pancreatic cancer, possibly through the regulation of EMT via the TGF‑β/Smad pathway and PVT1 may serve as a potential target for diagnostics and therapeutics in pancreatic cancer.

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