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Published on: July 21, 2018
CLK2 promotes occurrence and development of non-small cell lung cancer
Bing Liu1, Xiangshuo Kong, Rui Wang
1Department of Medical Oncology, Yantai Yuhuangding Hospital, Yantai, China.
Purpose:
To explore the role of CDC-like kinase 2 (CLK2) in the development and progression of lung cancer and its regulatory mechanism.
Methods:
Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assay was used to detect the expressions of micro ribonucleic acid (miR)-573 and CLK2 in non-small cell lung cancer (NSCLC) cell lines or tissues. The cell proliferative ability after overexpression of CLK2 was determined via cell counting kit-8 (CCK-8) and 5-Ethynyl-2'- deoxyuridine (EdU) assays. It was verified using dual-luciferase reporter assay and gain-loss assay that CLK2 was the target gene of miR-573, which was regulated by miR-573. According to the reverse assay, the effect of CLK2 on the proliferation of NSCLC cells was regulated by miR-573.
Results:
In qRT-PCR, the expression of CLK2 in NSCLC tissues and cell lines significantly rose. The CLK2 expression was increased in patients with stage Ⅲ-Ⅳ NSCLC and metastasis. According to survival analysis, highly-expressed CLK2 indicated a worse prognosis. The receiver operating characteristic (ROC) curves showed that CLK2 possessed the potential as a biomarker. It was found using the bioinformatics prediction that CLK2 was a potential target of miR-573. The results of dual-luciferase reporter assay confirmed that there was a binding relation between the two, and up-regulation of miR-573 could obviously inhibit the expression of CLK2. In qRT-PCR, the miR-573 expression in lung cancer tissues obviously declined, which was significantly negatively correlated with the expression of CLK2. CCK-8 and EdU assays manifested that the proliferation of lung cancer cells could be markedly enhanced through up-regulating CLK2. Finally, the results of reverse assay showed that up-regulating miR-573 could partially reverse the promoting effect of CLK2 on cell proliferation.
Conclusions:
Highly-expressed CLK2 significantly enhances the proliferation of lung cancer cells, thereby promoting the occurrence and development of lung cancer, which may be regulated by miR-573.
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