PMID- 32319575
OWN - NLM
STAT- MEDLINE
DCOM- 20210208
LR  - 20211204
IS  - 1791-2423 (Electronic)
IS  - 1019-6439 (Linking)
VI  - 56
IP  - 5
DP  - 2020 May
TI  - Uncoupling protein 2 is upregulated in melanoma cells and contributes to the 
      activation of Akt/mTOR and ERK signaling.
PG  - 1252-1261
LID - 10.3892/ijo.2020.5010 [doi]
AB  - The aim of the present study was to characterize the expression of uncoupling 
      protein 2 (UCP2) in melanoma and to study the potential mechanisms underlying the 
      involvement of UCP2 in melanomagenesis using human melanoma cell lines. The 
      expression of UCP2 was evaluated in specimens from normal control subjects, 
      patients with compound nevus, and patients with cutaneous and mucosal melanoma. 
      Stable knockdown of UCP2 was achieved in human melanoma cell lines, which were 
      used to examine whether UCP2 knockdown affects the mitochondrial membrane 
      potential and intracellular levels of ATP, reactive oxygen species and lactate. 
      Cell proliferation, invasion, spheroid formation and cisplatin sensitivity were 
      also evaluated in the UCP2 knockdown cells. Finally, the effects of UCP2 
      knockdown on the Akt/mammalian target of rapamycin (mTOR) and extracellular 
      signal‑regulated kinase (ERK) pathways, which are important oncogenic pathways 
      during melanomagenesis, were evaluated. Relatively high expression of UCP2 was 
      detected in human melanoma specimens, which was correlated with Clark level and 
      Breslow thickness. Knockdown of UCP2 suppressed cell proliferation, invasion and 
      spheroid formation, and increased the sensitivity of melanoma cells to cisplatin. 
      Furthermore, the UCP2 knockdown cells exhibited inhibition of Akt/mTOR signaling 
      and ERK activation. Therefore, human melanoma tissues exhibit relatively high 
      UCP2 expression, which may be implicated in the mechanisms underlying tumor 
      progression. The potential role of UCP2 in melanomagenesis may involve enhancing 
      the Akt/mTOR and mitogen‑activated protein kinase/ERK pathways.
FAU - Li, Jinran
AU  - Li J
AD  - Department of Dermatology, China‑Japan Union Hospital, Jilin University, 
      Changchun, Jilin 130033, P.R. China.
FAU - Jia, Yuxi
AU  - Jia Y
AD  - Department of Dermatology, China‑Japan Union Hospital, Jilin University, 
      Changchun, Jilin 130033, P.R. China.
FAU - An, Lin
AU  - An L
AD  - Department of Dermatology, China‑Japan Union Hospital, Jilin University, 
      Changchun, Jilin 130033, P.R. China.
FAU - Niu, Chunbo
AU  - Niu C
AD  - Department of Pathology, China‑Japan Union Hospital, Jilin University, Changchun, 
      Jilin 130033, P.R. China.
FAU - Cong, Xianling
AU  - Cong X
AD  - Department of Dermatology, China‑Japan Union Hospital, Jilin University, 
      Changchun, Jilin 130033, P.R. China.
FAU - Zhao, Yunfeng
AU  - Zhao Y
AD  - Department of Pharmacology, Toxicology and Neurosciences, LSU Health Sciences 
      Center, Shreveport, LA 71130, USA.
LA  - eng
PT  - Journal Article
DEP - 20200312
PL  - Greece
TA  - Int J Oncol
JT  - International journal of oncology
JID - 9306042
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (UCP2 protein, human)
RN  - 0 (Uncoupling Protein 2)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - Q20Q21Q62J (Cisplatin)
SB  - IM
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Cisplatin/pharmacology
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Gene Knockdown Techniques
MH  - Humans
MH  - MAP Kinase Signaling System
MH  - Male
MH  - Melanoma/drug therapy/genetics/*metabolism
MH  - Membrane Potential, Mitochondrial
MH  - Prognosis
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Uncoupling Protein 2/*genetics/*metabolism
MH  - *Up-Regulation
OTO - NOTNLM
OT  - uncoupling protein 2
OT  - melanoma
OT  - Akt
OT  - extracellular signal-regulated kinase
OT  - invasion
OT  - metabolism
EDAT- 2020/04/23 06:00
MHDA- 2021/02/09 06:00
CRDT- 2020/04/23 06:00
PHST- 2019/07/05 00:00 [received]
PHST- 2019/12/12 00:00 [accepted]
PHST- 2020/04/23 06:00 [pubmed]
PHST- 2021/02/09 06:00 [medline]
PHST- 2020/04/23 06:00 [entrez]
AID - 10.3892/ijo.2020.5010 [doi]
PST - ppublish
SO  - Int J Oncol. 2020 May;56(5):1252-1261. doi: 10.3892/ijo.2020.5010. Epub 2020 Mar 
      12.