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Research Paper|Volume 13, Issue 15|pp 19230—19242

LncRNA LINC01305 promotes cervical cancer progression through KHSRP and exosome-mediated transfer

Xianxia Huang1, Xuemei Liu1, Bo Du1, Xueling Liu1, Mei Xue1, Qingxin Yan1, Xiaohong Wang1, Qian Wang2
  • 1Department of Obstetrics and Gynecology, Jinan People’s Hospital Affiliated to Shandong First Medical University (Jinan City People’s Hospital), Jinan 271199, Shandong, P.R. China
  • 2Department of Obstetrics and Gynecology, the Fifth People's Hospital of Jinan, Jinan 250022, Shandong, P.R. China
Received: November 6, 2020Accepted: December 23, 2020Published: February 26, 2021
https://doi.org/10.18632/aging.202565

Copyright: © 2021 Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Cervical cancer (CC) is one of the deadliest female malignancies worldwide. Long non-coding RNAs (lncRNAs) are essential regulators for cancer progression. This study aimed to elucidate the role of lncRNA LINC01305 in the progression of CC. We found where LINC01305 was expressed in CC tissues and its correlation with the survival rate of CC patients. Functional experiments were performed to elucidate the effect of LINC01305 on CC. The results showed that LINC01305 was increased in CC tumor tissues and was correlated with a lower survival rate. The overexpression and knockdown of LINC01305 enhanced and inhibited the progression of CC, respectively. Additionally, the upregulation of LINC01305 promoted tumor growth in xenograft mice. Moreover, the effect of LINC01305 on CC was mediated through interacting with the RNA-binding protein, KHSRP. Furthermore, LINC01305 was mainly distributed in exosomes and was transferred to recipient cells to enhance CC progression. Lastly, LINC01305 may participate in the regulation of the stemness of CC. Taken together, the results suggest that LINC01305 promotes the progression of CC through KHSRP and that LINC01305 is released through exosomes and is involved in the stemness of CC. This study sheds light on the molecular mechanism underlying the progression of CC.