PMID- 32356935
OWN - NLM
STAT- MEDLINE
DCOM- 20220316
LR  - 20220719
IS  - 1752-8062 (Electronic)
IS  - 1752-8054 (Print)
IS  - 1752-8054 (Linking)
VI  - 15
IP  - 2
DP  - 2022 Feb
TI  - MicroRNA-100 Enhances Autophagy and Suppresses Migration and Invasion of Renal 
      Cell Carcinoma Cells via Disruption of NOX4-Dependent mTOR Pathway.
PG  - 567-575
LID - 10.1111/cts.12798 [doi]
AB  - Renal cell carcinoma (RCC) is the most common kidney malignancy and has a poor 
      prognosis owing to its resistance to chemotherapy. Recently, microRNAs (miRNAs or 
      miRs) have been shown to have a role in cancer metastasis and potential as 
      prognostic biomarkers in cancer. In the present study, we aim to explore the 
      potential role of miR-100 in RCC by targeting nicotinamide adenine dinucleotide 
      phosphate oxidase 4 (NOX4) through the mammalian target of rapamycin (mTOR) 
      pathway. Initially, microarray-based gene expression profiling of RCC was used to 
      identify differentially expressed genes. Next, the expression of miR-100 and NOX4 
      was examined in RCC tissues and cell lines. Then, the interaction between miR-100 
      and NOX4 was identified using bioinformatics analysis and dual-luciferase 
      reporter assay. Gain-of-function or loss-of-function approaches were adopted to 
      manipulate miR-100 and NOX4 in order to explore the functional roles in RCC. The 
      results revealed the presence of an upregulated NOX4 and a downregulated miR-100 
      in both RCC tissues and cell lines. NOX4 was verified as a target of miR-100 in 
      cells. In addition, overexpression of miR-100 or NOX4 silencing could increase 
      autophagy while decreasing the expression of mTOR pathway-related genes and 
      migration and invasion. Conjointly, upregulated miR-100 can potentially increase 
      the autophagy and inhibit the invasion and migration of RCC cells by targeting 
      NOX4 and inactivating the mTOR pathway, which contributes to an extensive 
      understanding of RCC and may provide novel therapeutic options for this disease.
CI  - (c) 2020 The Authors. Clinical and Translational Science published by Wiley 
      Periodicals LLC on behalf of the American Society of Clinical Pharmacology and 
      Therapeutics.
FAU - Liu, Xiumin
AU  - Liu X
AD  - Department of Clinical Laboratory, The Second Hospital of Jilin University, 
      Changchun, China.
FAU - Zhong, Lili
AU  - Zhong L
AD  - Jilin Provincial Key Laboratory on Molecular and Chemical Genetic, The Second 
      Hospital of Jilin University, Changchun, China.
FAU - Li, Ping
AU  - Li P
AD  - Department of Developmental Pediatrics, The Second Hospital of Jilin University, 
      Changchun, China.
FAU - Zhao, Peng
AU  - Zhao P
AD  - Department of Anesthesiology, The Second Hospital of Jilin University, Changchun, 
      China.
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20200625
PL  - United States
TA  - Clin Transl Sci
JT  - Clinical and translational science
JID - 101474067
RN  - 0 (MIRN100 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - EC 1.6.3.- (NADPH Oxidase 4)
RN  - EC 1.6.3.- (NOX4 protein, human)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - W36ZG6FT64 (Sirolimus)
SB  - IM
ECI - Clin Transl Sci. 2022 Jan 17;:. PMID: 35040255
MH  - Autophagy/genetics
MH  - *Carcinoma, Renal Cell/genetics/metabolism/pathology
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - *Kidney Neoplasms/genetics
MH  - *MicroRNAs/genetics
MH  - NADPH Oxidase 4/genetics/metabolism
MH  - Sirolimus
MH  - TOR Serine-Threonine Kinases/genetics/metabolism
PMC - PMC8841407
COIS- The authors declared no competing interests for this work.
EDAT- 2020/05/02 06:00
MHDA- 2022/03/17 06:00
PMCR- 2022/02/01
CRDT- 2020/05/02 06:00
PHST- 2019/12/23 00:00 [received]
PHST- 2020/03/04 00:00 [accepted]
PHST- 2020/05/02 06:00 [pubmed]
PHST- 2022/03/17 06:00 [medline]
PHST- 2020/05/02 06:00 [entrez]
PHST- 2022/02/01 00:00 [pmc-release]
AID - CTS12798 [pii]
AID - 10.1111/cts.12798 [doi]
PST - ppublish
SO  - Clin Transl Sci. 2022 Feb;15(2):567-575. doi: 10.1111/cts.12798. Epub 2020 Jun 
      25.