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LINC00511 knockdown prevents cervical cancer cell proliferation and reduces resistance to paclitaxel
- Mao, Ben-Di, Xu, Ping, Zhong, Yan, Ding, Wei-Wei, Meng, Qing-Zhi
- Journal of biosciences 2019 v.44 no.2 pp. 44
- P-glycoproteins, apoptosis, cell lines, cell proliferation, cell viability, drug resistance, drug therapy, females, gelatinase A, interphase, lymph nodes, metastasis, neoplasm cells, non-coding RNA, paclitaxel, patients, uterine cervical neoplasms
- Cervical cancer (CC) is one of the most common female malignancies in the world. Although paclitaxel (PTX) is a critical chemotherapy agent for the treatment of CC, its treatment outcome is limited by the development of drug resistance. The present study aims to define the role of long non-coding RNA (lncRNA) LINC00511 in the progression of CC with the involvement of cell proliferation, apoptosis and resistance to PTX in Hela/PTX cells. CC and adjacent normal tissue samples were collected from 84 patients with CC, and used to determine LINC0051 expression. PTX-resistant Hela/PTX cell line was constructed, in which LINC0051 was overexpressed or silenced to further investigate the effect of LINC00511 on PTX-resistant Hela/PTX cell viability, proliferation, migration, invasion, cell cycle, apoptosis and resistance of CC cells to PTX. The expression of Bcl-2, Bax, cleaved-caspase-3, matrix metalloproteinase (MMP)-2, MMP-9, multidrug resistance protein 1 (MRP1) and P-glycoprotein (P-GP) was also assessed. High-expression of LINC00511 was found in CC with its close association with the tumor stage, tumor size and lymph node metastasis. After silencing LINC00511 expression, the expression of MRP1, P-GP, Bcl-2, MMP-2 and MMP-9 was decreased, while Bax and cleaved-caspase-3 increased with more CC cells arrested at G1 phase. Furthermore, silencing of LINC00511 could suppress cell resistance to PTX, cell viability, cell proliferation, migration and invasion yet promoted cell apoptosis in PTX-resistant Hela/PTX cells. Collectively, our findings demonstrate that silencing of LINC00511 could inhibit CC cell resistance to PTX, cell proliferation, migration and invasion, and promote cell apoptosis in CC. Silencing of LINC00511 provides a novel therapeutic target for CC.