| Literature DB >> 28391028 |
Lili Qian1, Fei Xu1, Xiaolin Wang2, Ming Jiang2, Juan Wang1, Weiguo Song1, Dabao Wu1, Zhen Shen1, Dingqing Feng3, Bin Ling3, Yong Cheng4, Weihua Xiao5, Ge Shan6, Ying Zhou7.
Abstract
We aim to determine the lncRNA targets of ΔNp63α in cervical cancer and molecular programs in cancerous differentiation. Different profiles of the lncRNAs were assayed and validated in overexpressing p63 SiHa cells (SiHa/ΔNp63α) and the control cell lines (SiHa/pCon). ENST00000422259, ENST00000447565 (Lnc-LIF-AS) and ENST00000469965, together with their related antisense mRNA DPYD (dihydropyrimidine dehydrogenase, a pyrimidine catabolic pathway gene), LIF (leukemia inhibitor factor) and FLNC (filamin C) were all notably differentially expressed in both ΔNp63α overexpression cells and knockdown cells. Here, we illustrated that ΔNp63α can inhibit the levels of LIF mRNA by direct transcription regulation and decrease LIF mRNA stability by suppressing the expression of Lnc-LIF-AS. An inverse interaction of LIF and ΔNp63α expression was as well validated in clinical samples of cervical cancer, and high level of LIF in cervical cancers was related with poor patient survival. The decrease of ΔNp63α also attenuated the differentiation of cervical cancerous cells. Suggesting that ΔNp63α may be form a complex network in regulation cervical cancerous differentiation.Entities:
Keywords: Cervical cancer; LIF; LncRNA; ΔNp63α
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Year: 2017 PMID: 28391028 DOI: 10.1016/j.cyto.2017.04.001
Source DB: PubMed Journal: Cytokine ISSN: 1043-4666 Impact factor: 3.861