Neoplasma Vol.69, No.6, p. 1406–1417, 2022
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| Title: LncRNA CBR3-AS1 predicts a poor prognosis and promotes cervical cancer progression through the miR-3163/LASP1 pathway |
| Author: Yi-Pin CAI, Yu HUANG, Jie ZHANG, Xiao-Li LIU, Fang ZHAO, Kuan ZHANG, Song-Yuan XU, Yan YANG, Hai-Wei HUANG, Yu GAO |
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Abstract: LncRNA carbonyl reductase antisense RNA 1 (CBR3-AS1) is increased in cervical cancer and predicts poor prognosis. This study aims to investigate the underlying mechanism of lncRNA CBR3-AS1 in cervical cancer. LncRNA CBR3-AS1 and LASP1 expressions were significantly elevated in cervical cancer tissue and cells, whereas miR-3163 expression was significantly decreased in cervical cancer tissue and cells. High lncRNA CBR3-AS1 expression and LASP1 expression showed a lower overall survival rate, whereas high miR-3163 expression showed a higher overall survival rate. Correlation between clinicopathological parameters of cervical cancer patients and lncRNA CBR3-AS1, miR-3163, LASP1 expressions indicated that the expressions of lncRNA CBR3-AS1, miR-3163, and LASP1 were closely related with distant metastasis and lymphatic metastasis of cervical cancer. LncRNA CBR3-AS1 knockdown suppressed cervical cancer cell viability and inhibited cancer stem cell-like properties. Besides, we identified that lncRNA CBR3-AS1 interacted with miR-3163, and miR-3163 targeted to LASP1. Moreover, the correlation between lncRNA CBR3-AS1 and miR-3163, as well as the correlation between miR-3163 and LASP1 was confirmed. Finally, lncRNA CBR3-AS1 knockdown inhibited tumor growth and suppressed cancer stem cell-like properties of cervical cancer in vivo. Taken together, high expression of lncRNA CBR3-AS1 predicts poor prognosis in cervical cancer, and the lncRNA CBR3-AS1/miR-3163/LASP1 pathway plays a vital function in the modulation of cervical cancer cell proliferation and cancer stem cell-like properties.
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| Keywords: lncRNA CBR3-AS1, miR-3163, LASP1, proliferation, cancer stem cell-like properties, poor prognosis |
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Published online: 30-Dec-2022
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| Year: 2022, Volume: 69, Issue: 6 |
Page From: 1406, Page To: 1417 |
doi:10.4149/neo_2022_220730N784
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