IMR Press / FBL / Volume 25 / Issue 5 / DOI: 10.2741/4842

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

PCAT1/miR-129/ABCB1 axis confers chemoresistance in non-small cell lung cancer
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1 Department of respiration, Shanxi Tumour Hospital, Taiyuan 030013, Shanxi Province, China
2 Medical Oncology, the First Affiliated Hospital of Anhui Medical University; Hefei 230022, Anhui Province, China
3 Cardiothoracic surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
Send correspondence to: Huanwen Chen, Cardiothoracic surgery, the First Affiliated Hospital of Chongqing Medical University, No.1 Youyi Road, Yuzhong District, Chongqing 400016, China, Tel: 86-023-89012238, Fax: 02365102346, E-mail:
Front. Biosci. (Landmark Ed) 2020, 25(5), 948–960;
Published: 1 March 2020
(This article belongs to the Special Issue Leader sequences of coronavirus are altered during infection)

Long noncoding RNA prostate cancer-associated transcript 1 (PCAT1) is oncogenic and causes progression of non-small cell lung cancer (NSCLC). We hypothesized that PCAT1 might be involved in the acquisition of chemoresistance of NSCLC cells to treatment with cisplatin (DDP). Here, we show that PCAT1 and ATP-binding cassette sub-family B member 1 (ABCB1) are highly expressed in NSCLC tissues and cell lines, and regulate the growth and apoptosis of these cells. Compared with those in DDP-sensitive patients, PCAT1 and ABCB1 are highly expressed in the tumors of DDP-resistant patients, and such overexpression correlates with a shorter overall survival of these patients. Knockdown of PCAT1 or upregulation of miR-129 led to apoptosis and sensitized the DDP-resistant cells to DDP. The 3’ UTR activity of PCAT1 and ABCB1, which was increased by PCAT1 overexpression, was shown to harbor an miR-129 binding site. DDP resistance is induced by elevated ABCB1 expression, which involves binding of miR-129 in DDP resistant cells. These findings suggest that the PCAT1/miR-129/ABCB1 axis may be a potential target for the treatment of DDP-resistant oat cell cancer.

Non-Small Cell Lung Cancer
Prostate Cancer-Associated Transcript 1
ATP-Binding Cassette Sub-Family B member 1
Figure 1
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