UCH‐L3 promotes non‐small cell lung cancer proliferation via accelerating cell cycle and inhibiting cell apoptosis.

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Bibliographic Details
Title:	UCH‐L3 promotes non‐small cell lung cancer proliferation via accelerating cell cycle and inhibiting cell apoptosis.
Authors:	Li, Guoping¹ (AUTHOR), Jin, Xiaosheng¹ (AUTHOR), Zheng, Jisheng¹ (AUTHOR), Jiang, Na¹ (AUTHOR), Shi, Wang² (AUTHOR) WangShifgh@163.com
Source:	Biotechnology & Applied Biochemistry. Feb2021, Vol. 68 Issue 1, p165-172. 8p.
Subjects:	Cell cycle, Cancer cell proliferation, Inhibition of cellular proliferation, Cell proliferation, Lung cancer
Abstract:	Ubiquitin C‐terminal hydrolase‐L3 (UCH‐L3) is a deubiquitinase that has a crucial role in oncogenesis. This study was aimed to explore the biological function of UCH‐L3 in non‐small cell lung cancer (NSCLC). Bioinformatics analysis was used to detect UCH‐L3 expression in NSCLC tissues and normal lung tissues, and to analyze the relationship between UCH‐L3 expression and survival of patients. qRT‐PCR and western blotting assays were used to detect UCH‐L3 expression in NSCLC tumor tissues and adjacent normal tissues. CCK‐8 assay was performed to examine the effect of UCH‐L3 on NSCLC cell proliferation. Flow cytometry assay was conducted to examine the effect of UCH‐L3 on NSCLC cell cycle and apoptosis. The expression of UCH‐L3 in NSCLC tissues was markedly higher than in normal lung tissues, and high expression of UCH‐L3 was positively associated with the poor survival of patients. UCH‐L3 knockdown significantly inhibited the proliferation of NSCLC cells, whereas UCH‐L3 overexpression had the opposite effect. Moreover, UCH‐L3 promoted NSCLC cells proliferation via accelerating cell cycle and inhibiting cell apoptosis. UCH‐L3 is upregulated in NSCLC and positively associated with the poor survival, and its expression contributes to NSCLC cell proliferation by accelerating cell cycle and inhibiting cell apoptosis. [ABSTRACT FROM AUTHOR]
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Database:	Engineering Source

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Abstract:	Ubiquitin C‐terminal hydrolase‐L3 (UCH‐L3) is a deubiquitinase that has a crucial role in oncogenesis. This study was aimed to explore the biological function of UCH‐L3 in non‐small cell lung cancer (NSCLC). Bioinformatics analysis was used to detect UCH‐L3 expression in NSCLC tissues and normal lung tissues, and to analyze the relationship between UCH‐L3 expression and survival of patients. qRT‐PCR and western blotting assays were used to detect UCH‐L3 expression in NSCLC tumor tissues and adjacent normal tissues. CCK‐8 assay was performed to examine the effect of UCH‐L3 on NSCLC cell proliferation. Flow cytometry assay was conducted to examine the effect of UCH‐L3 on NSCLC cell cycle and apoptosis. The expression of UCH‐L3 in NSCLC tissues was markedly higher than in normal lung tissues, and high expression of UCH‐L3 was positively associated with the poor survival of patients. UCH‐L3 knockdown significantly inhibited the proliferation of NSCLC cells, whereas UCH‐L3 overexpression had the opposite effect. Moreover, UCH‐L3 promoted NSCLC cells proliferation via accelerating cell cycle and inhibiting cell apoptosis. UCH‐L3 is upregulated in NSCLC and positively associated with the poor survival, and its expression contributes to NSCLC cell proliferation by accelerating cell cycle and inhibiting cell apoptosis. [ABSTRACT FROM AUTHOR]
ISSN:	08854513
DOI:	10.1002/bab.1909