Universität zu Köln

Zhu, Yaru, Shen, Yefeng, Chen, Rui, Li, Hui, Wu, Yuanzhou, Zhang, Fuwei, Huang, Weimei, Guo, Linlang, Chen, Qunqing and Liu, Huanxin (2021). KCNQ1OT1 lncRNA affects the proliferation, apoptosis, and chemoresistance of small cell lung cancer cells via the JAK2/STAT3 axis. ANN. TRANSL. MED., 9 (10). SHATIN: AME PUBL CO. ISSN 2305-5847

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Abstract

Background: Small cell lung cancer (SCLC) is a devastating and aggressive neuroendocrine carcinoma characterized by high cellular proliferation and early metastatic spread. Numerous studies have demonstrated that long noncoding RNAs (lncRNAs) can regulate tumor generation and development, including in SCLC. The current study aimed to assess the effect of the lncRNA, KCNQ1OT1, on the proliferation, apoptosis, and chemoresistance of SCLC and the potential underlying molecular mechanism. Methods: Matched chemo-resistant and sensitive cells were applied to RNA isolation and followed by expression profiling by microarray analysis and subsequent quantitative polymerase chain reaction (qPCR) validation. Cell viability and apoptosis were determined by Cell Counting Kit-8 and flow cytometry to examine the chemoresistance and apoptosis of KCNQ1OT1 knockdown with lentivirus-mediated RNA interference. Furthermore, cell proliferation was studied by colony formation, and invasion and migration were tested by Transwell cell invasion and wound-healing assays, respectively. A tumor xenograft model was established to determine the role of KCNQ1OT1 in tumor growth and chemoresistance in response to KCNQ1OT1 knockdown in vivo. Western blot analysis, qPCR, and immunohistochemistry were used to detect the levels of messenger RNA (mRNA) Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway-related markers. Results: Higher expression of KCNQ1OT1 was detected in SCLC chemo-resistant verso chemo-sensitive cells. Knockdown of KCNQ1OT1 inhibited SCLC cell viability and cloning ability, hindered cell migration and invasion, induced apoptosis in vitro, and suppressed tumor growth and chemoresistance in vivo, by activating the JAK2/STAT3 signaling pathway. Conclusions: This is the first study to indicate that lncRNA KCNQ1OT1 promotes cell proliferation and invasion, and prevents apoptosis of SCLC by activating the JAK2/STAT3 pathway.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Zhu, Yaru UNSPECIFIED UNSPECIFIED UNSPECIFIED Shen, Yefeng UNSPECIFIED UNSPECIFIED UNSPECIFIED Chen, Rui UNSPECIFIED UNSPECIFIED UNSPECIFIED Li, Hui UNSPECIFIED UNSPECIFIED UNSPECIFIED Wu, Yuanzhou UNSPECIFIED UNSPECIFIED UNSPECIFIED Zhang, Fuwei UNSPECIFIED UNSPECIFIED UNSPECIFIED Huang, Weimei UNSPECIFIED UNSPECIFIED UNSPECIFIED Guo, Linlang UNSPECIFIED UNSPECIFIED UNSPECIFIED Chen, Qunqing UNSPECIFIED UNSPECIFIED UNSPECIFIED Liu, Huanxin UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-582379
DOI:	10.21037/atm-21-1761
Journal or Publication Title:	ANN. TRANSL. MED.
Volume:	9
Number:	10
Date:	2021
Publisher:	AME PUBL CO
Place of Publication:	SHATIN
ISSN:	2305-5847
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language REGULATES PROLIFERATION; RESISTANCE; TUMORIGENESIS; MIGRATION; PROMOTES Multiple languages Oncology; Medicine, Research & Experimental Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/58237