LINC00511 knockdown prevents cervical cancer cell proliferation and reduces resistance to paclitaxel

Cervical cancer (CC) is one of the most common female malignancies in the world. Although paclitaxel (PTX) is a criticalchemotherapy agent for the treatment of CC, its treatment outcome is limited by the development of drug resistance. Thepresent study aims to define the role of long non-coding RNA (lncRNA) LINC00511 in the progression of CC with theinvolvement of cell proliferation, apoptosis and resistance to PTX in Hela/PTX cells. CC and adjacent normal tissuesamples were collected from 84 patients with CC, and used to determine LINC0051 expression. PTX-resistant Hela/PTXcell line was constructed, in which LINC0051 was overexpressed or silenced to further investigate the effect of LINC00511on PTX-resistant Hela/PTX cell viability, proliferation, migration, invasion, cell cycle, apoptosis and resistance of CC cellsto 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 CCwith its close association with the tumor stage, tumor size and lymph node metastasis. After silencing LINC00511expression, the expression of MRP1, P-GP, Bcl-2, MMP-2 and MMP-9 was decreased, while Bax and cleaved-caspase-3increased with more CC cells arrested at G1 phase. Furthermore, silencing of LINC00511 could suppress cell resistance toPTX, 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 therapeutictarget for CC.