PMID- 37539493
OWN - NLM
STAT- MEDLINE
DCOM- 20230912
LR  - 20231213
IS  - 1582-4934 (Electronic)
IS  - 1582-1838 (Print)
IS  - 1582-1838 (Linking)
VI  - 27
IP  - 18
DP  - 2023 Sep
TI  - SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through 
      the AKT1/mTOR pathway.
PG  - 2675-2683
LID - 10.1111/jcmm.17844 [doi]
AB  - Spi-1 proto-oncogene (SPI1) plays a vital role in carcinogenesis. Our work aimed 
      to investigate the potential regulatory mechanism of SPI1 in melanoma. The mRNA 
      and protein levels were measured via qRT-PCR and Western blotting. Cell viability 
      was assessed by CCK-8 assay. The target relationship between SPI1 and hexokinase 
      2 (HK2) was determined using dual-luciferase reporter detection. ChIP was 
      conducted to confirm the targeted relationship between SPI1 and the HK2 promoter. 
      Immunohistochemistry analysis was conducted to measure the positive cell number 
      of SPI1 and HK2 in melanoma tissues. The cell migration abilities were determined 
      using a wound healing assay. Glucose consumption, pyruvate dehydrogenase 
      activity, lactate production and ATP levels were measured to assess glycolysis. 
      SPI1 transcription in melanoma cells and tissues was dramatically higher than 
      that in adjacent normal tissues and epidermal melanocyte HEMa-LP, respectively. 
      Knockdown of SPI1 restrained cell viability, metastasis and glycolysis in 
      melanoma cells. SPI1 directly targeted HK2, and knockdown of SPI1 repressed HK2 
      expression. Overexpression of HK2 weakened the inhibitory effects of SPI1 
      knockdown on the viability, metastasis and glycolysis of melanoma cells. The 
      serine-threonine kinase 1 (AKT1)/mammalian target of rapamycin (mTOR) axis is 
      involved in melanoma progression. SPI1 knockdown restrained melanoma cell 
      proliferation, metastasis and glycolysis by regulating the AKT1/mTOR pathway.
CI  - (c) 2023 The Authors. Journal of Cellular and Molecular Medicine published by 
      Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
FAU - Liu, Chunlei
AU  - Liu C
AD  - Department of dermatology, Xiangyang No.1 People's Hospital, Hubei University of 
      Medicine, Xiangyang, China.
FAU - Qiu, Xiujuan
AU  - Qiu X
AD  - Department of oncology, Xiangyang No.1 People's Hospital, Hubei University of 
      Medicine, Xiangyang, China.
FAU - Gao, Jun
AU  - Gao J
AD  - Department of general surgury, Xiangyang No.1 People's Hospital, Hubei University 
      of Medicine, Xiangyang, China.
FAU - Gong, Zhifan
AU  - Gong Z
AD  - Department of dermatology, Xiangyang No.1 People's Hospital, Hubei University of 
      Medicine, Xiangyang, China.
FAU - Zhou, Xiaogang
AU  - Zhou X
AD  - Department of dermatology, Xiangyang No.1 People's Hospital, Hubei University of 
      Medicine, Xiangyang, China.
FAU - Luo, Haichao
AU  - Luo H
AD  - Department of oncology, Xiangyang No.1 People's Hospital, Hubei University of 
      Medicine, Xiangyang, China.
FAU - Geng, Xuerui
AU  - Geng X
AUID- ORCID: 0000-0002-4591-9235
AD  - Department of dermatology, Xiangyang No.1 People's Hospital, Hubei University of 
      Medicine, Xiangyang, China.
LA  - eng
PT  - Journal Article
DEP - 20230804
PL  - England
TA  - J Cell Mol Med
JT  - Journal of cellular and molecular medicine
JID - 101083777
RN  - 0 (MicroRNAs)
RN  - EC 2.7.1.1 (Hexokinase)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (AKT1 protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Humans
MH  - *MicroRNAs/genetics
MH  - Hexokinase/genetics/metabolism
MH  - TOR Serine-Threonine Kinases/genetics/metabolism
MH  - *Melanoma/genetics/pathology
MH  - Cell Proliferation/genetics
MH  - Cell Line, Tumor
MH  - Proto-Oncogene Proteins c-akt/genetics/metabolism
MH  - Melanoma, Cutaneous Malignant
PMC - PMC10494286
OTO - NOTNLM
OT  - AKT1/mTOR pathway
OT  - SPI-1 proto-oncogene (SPI1)
OT  - glycolysis
OT  - hexokinase 2 (HK2)
OT  - melanoma
COIS- The authors declare that they have no conflicts of interest.
EDAT- 2023/08/04 06:43
MHDA- 2023/09/12 06:41
PMCR- 2023/08/04
CRDT- 2023/08/04 04:43
PHST- 2023/06/25 00:00 [revised]
PHST- 2022/12/09 00:00 [received]
PHST- 2023/06/30 00:00 [accepted]
PHST- 2023/09/12 06:41 [medline]
PHST- 2023/08/04 06:43 [pubmed]
PHST- 2023/08/04 04:43 [entrez]
PHST- 2023/08/04 00:00 [pmc-release]
AID - JCMM17844 [pii]
AID - 10.1111/jcmm.17844 [doi]
PST - ppublish
SO  - J Cell Mol Med. 2023 Sep;27(18):2675-2683. doi: 10.1111/jcmm.17844. Epub 2023 Aug 
      4.