miRNA-148a inhibits cell growth of papillary thyroid cancer through STAT3 and PI3K/AKT signaling pathways
Author(s) -
Yuan Xu,
Yifan Han,
Shaojun Zhu,
Jianda Dong,
Bing Ye
Publication year - 2017
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.2017.5947
Subject(s) - papillary thyroid cancer , cancer research , thyroid cancer , pi3k/akt/mtor pathway , protein kinase b , cell growth , cancer , apoptosis , microrna , oncogene , biology , stat3 , cell cycle , cancer cell , signal transduction , pathology , medicine , microbiology and biotechnology , biochemistry , gene
The function of miRNA‑148a in lymphatic metastases of papillary thyroid cancer and its mechanism were tested. In this investigation, miRNA‑148a expression of lymphatic metastases of papillary thyroid cancer patients was inhibited, compared with normal group. We found that miRNA‑148a overexpression was effectively reduced cell cell proliferation and metastases, and induced apoptosis of papillary thyroid cancer in vitro. Overexpression of miRNA‑148a significantly induced Bax protein expression and caspase‑3/9 levels, and suppressed phosphorylation STAT3 (p‑STAT3), PI3K and p‑Akt protein expression of papillary thyroid cancer in vitro. Next, si‑STAT3, could inhibit p‑STAT3 protein expression, reducing cell-cell proliferation and metastases, and inducing apoptosis of papillary thyroid cancer following miRNA‑148a overexpression. Then, the PI3K inhibitor was able to inhibit PI3K and p‑Akt protein expression, reduced cell cell proliferation and metastases, and induced apoptosis of papillary thyroid cancer following miRNA‑148a overexpression. Taken together, our results suggest that miRNA‑148a inhibits lymphatic metastases of papillary thyroid cancer through STAT3 and PI3K/AKT signaling pathways.
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