Home HOME Neoplasma 2021 Neoplasma Vol.68, No.2, p.334–341, 2021

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Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

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Neoplasma Vol.68, No.2, p.334–341, 2021

Title: Abnormal expression of lncRNA UCA1 disturbed cell apoptosis through mediating mitochondrial dynamics in PDAC
Author: BuWei Teng, Tao Feng, Wei Li, Zhong Wang

Abstract: A great number of studies have shown the pivotal role of mitochondria in cancer progression and numerous studies indicated that lncRNAs are involved in tumor metabolism. However, the relationship between UCA1 and mitochondria in PDAC remains unclear. Here, we reported for the first time that UCA1-driven change in mitochondrial dynamics induced mitochondrial apoptotic pathway in PDAC. In this research, data mining revealed that upregulated UCA1 occurred in PDAC patients, which meant a high likelihood of a poor prognosis. Following, UCA1 silencing could notably decrease cell viability and induce cell apoptosis. Further research revealed that UCA1 silencing could induce more cytochrome c localization in the cytosol, which triggered the mitochondrial apoptotic pathway in PDAC cell lines. Meanwhile, the morphological analysis showed significantly enhanced mitochondrial fragmentation presented in UCA1 knockdown cells, coupled with increased expression of Drp1 and Fis1, together with activation form of Drp1, which would promote mitochondria fission. Additional, mitochondrial fission inhibitor Mdivi1 markedly reversed the effects of the UCA1 knockdown on cell apoptosis in PDAC. Collectively, we deduce that UCA1-driven change in mitochondrial dynamics induced mitochondrial apoptotic pathway in PDAC. Therefore, lncRNA UCA1 could be considered as a promising therapeutic target for the poor prognosis in PDAC.

Keywords: long non‑coding RNA UCA1; pancreatic ductal adenocarcinoma; mitochondrial dynamics; mitochondrial apoptotic pathway
Published online: 22-Dec-2020
Year: 2021, Volume: 68, Issue: 2 Page From: 334, Page To: 341

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