PMID- 32047545
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 1837-9664 (Print)
IS  - 1837-9664 (Electronic)
IS  - 1837-9664 (Linking)
VI  - 11
IP  - 6
DP  - 2020
TI  - Long non-coding RNA TCL6 enhances preferential toxicity of paclitaxel to renal 
      cell carcinoma cells.
PG  - 1383-1392
LID - 10.7150/jca.32552 [doi]
AB  - Background: Recent findings have shown long non-coding RNAs (lncRNAs) are 
      dysregulated in a variety of cancer cells. In this report, we investigate the 
      effect of T-cell leukemia lymphoma 6 (TCL6) on paclitaxel (PTX)-induced apoptosis 
      in Renal cell carcinoma (RCC) cells. Methods: Expression levels of TCL6 in RCC 
      tissues were analyzed via The Cancer Genome Atlas (TCGA) and Gene Expression 
      Omnibus (GEO) datasets. Fluorescence in situ hybridization (FISH) was performed 
      to detect the expression of TCL6 in RCC tissues and cells. Two pairs of cell 
      lines were used: TCL6-silenced 786-O cell line and scrambled 786-O cell line, 
      TCL6-overexpressed Caki-1 cell line and Caki-1 scrambled cell line. Cell 
      viability was detected using the MTT assay. Apoptosis was examined by flow 
      cemetery. Dual reporter gene assay was performed to confirm the direct downstream 
      target miRNA of TCL6. Results: Based on RNA sequencing expression data of RCC 
      tissues from TCGA and GEO datasets, the expression deficiency of TCL6 was 
      observed in RCC tissues. Low level of TCL6 was associated with worse overall and 
      disease-free survival of RCC patients. The FISH showed similar results with low 
      expression of TCL6 in RCC tissues and cells. After PTX treatment, a 
      time-dependent decrease in cell viability was observed in TCL6-overexpressed RCC 
      cells and an increase in cell viability was observed in TCL6-silenced cells 
      compared to control cells. Apoptosis induced by PTX was significantly increased 
      in TCL6-overexpressed cells. Inhibition of TCL6 showed a significant decrease in 
      apoptosis. Furthermore, luciferase reporter assay revealed that TCL6 is a direct 
      target gene of miR-221. Conclusions: TCL6 effectively sensitizes RCC to PTX 
      mainly through downregulation of miR-221. Our results suggest that PTX combined 
      with TCL6 might be a potentially more effective chemotherapeutic approach for 
      renal cancer.
CI  - (c) The author(s).
FAU - Chen, Zhizhao
AU  - Chen Z
AD  - The Third Xiangya Hospital of Central South University, Changsha, China.
AD  - Wuhan University, Zhongnan Hospital of Wuhan University, Institute of 
      Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan 
      University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan 
      Hubei, China.
FAU - Zhuang, Quan
AU  - Zhuang Q
AD  - The Third Xiangya Hospital of Central South University, Changsha, China.
FAU - Cheng, Ke
AU  - Cheng K
AD  - The Third Xiangya Hospital of Central South University, Changsha, China.
FAU - Ming, Yingzi
AU  - Ming Y
AD  - The Third Xiangya Hospital of Central South University, Changsha, China.
FAU - Zhao, Yujun
AU  - Zhao Y
AD  - The Third Xiangya Hospital of Central South University, Changsha, China.
FAU - Ye, Qifa
AU  - Ye Q
AD  - The Third Xiangya Hospital of Central South University, Changsha, China.
AD  - Wuhan University, Zhongnan Hospital of Wuhan University, Institute of 
      Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan 
      University, Hubei Key Laboratory of Medical Technology on Transplantation, Wuhan 
      Hubei, China.
FAU - Zhang, Sheng
AU  - Zhang S
AD  - The Third Xiangya Hospital of Central South University, Changsha, China.
LA  - eng
PT  - Journal Article
DEP - 20200101
PL  - Australia
TA  - J Cancer
JT  - Journal of Cancer
JID - 101535920
PMC - PMC6995388
OTO - NOTNLM
OT  - Apoptosis
OT  - Chemotherapy.
OT  - Paclitaxel
OT  - Renal cell carcinoma
COIS- Competing Interests: The authors have declared that no competing interest exists.
EDAT- 2020/02/13 06:00
MHDA- 2020/02/13 06:01
PMCR- 2020/01/01
CRDT- 2020/02/13 06:00
PHST- 2018/12/24 00:00 [received]
PHST- 2019/10/26 00:00 [accepted]
PHST- 2020/02/13 06:00 [entrez]
PHST- 2020/02/13 06:00 [pubmed]
PHST- 2020/02/13 06:01 [medline]
PHST- 2020/01/01 00:00 [pmc-release]
AID - jcav11p1383 [pii]
AID - 10.7150/jca.32552 [doi]
PST - epublish
SO  - J Cancer. 2020 Jan 1;11(6):1383-1392. doi: 10.7150/jca.32552. eCollection 2020.