PMID- 34091441
OWN - NLM
STAT- MEDLINE
DCOM- 20210722
LR  - 20211204
IS  - 1945-4589 (Electronic)
IS  - 1945-4589 (Linking)
VI  - 13
IP  - 10
DP  - 2021 Apr 21
TI  - E2F2 inhibition induces autophagy via the PI3K/Akt/mTOR pathway in gastric 
      cancer.
PG  - 13626-13643
LID - 10.18632/aging.202891 [doi]
AB  - BACKGROUND: E2F2 is a member of the E2F transcription factor family and has 
      important but not fully understood biological functions in cancers. The 
      biological role of E2F2 in gastric cancer (GC) also remains unclear. METHODS: We 
      examined the expression levels of E2F2 in GC using publicly available datasets 
      such as TIMER, Oncomine, GEPIA, UALCAN, etc., and in our patient cohort, using 
      quantitative real-time PCR, western blotting, and immunohistochemistry. We 
      further investigated the effects of E2F2 on phosphatidylinositol 3-kinase 
      (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling, autophagy, and the 
      migration and invasion of GC cells by the wound healing assay, Transwell assay 
      and transmission electron microscopy. RESULTS: E2F2 was highly expressed in both 
      GC tissues and cells compared with normal gastric tissues/cells. High E2F2 
      expression was associated with poor overall survival (OS). In addition, the 
      expression of E2F2 in GC was strongly correlated with a variety of immune 
      markers. E2F2 overexpression promoted the migration and invasiveness of GC cells 
      in vitro through inhibition of PI3K/Akt/mTOR-mediated autophagy. CONCLUSION: High 
      E2F2 expression was associated with the characteristics of invasive tumors and 
      poor prognosis. E2F2 also had potential modulatory effects on tumor immunity. We 
      discovered a novel function of E2F2 in the regulation of PI3K/Akt/mTOR-mediated 
      autophagy and the downstream processes of cell migration and invasion.
FAU - Li, Hui
AU  - Li H
AD  - Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong, China.
FAU - Zhao, Shufen
AU  - Zhao S
AD  - Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong, China.
FAU - Shen, Liwei
AU  - Shen L
AD  - Department of Oncology, Qingdao Women and Children's Hospital, Qingdao, Shandong, 
      China.
FAU - Wang, Peige
AU  - Wang P
AD  - Department of Emergency Surgery, The Affiliated Hospital of Qingdao University, 
      Qingdao, Shandong, China.
FAU - Liu, Shihai
AU  - Liu S
AD  - Central Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong, China.
FAU - Ma, Yingji
AU  - Ma Y
AD  - Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong, China.
FAU - Liang, Zhiwei
AU  - Liang Z
AD  - Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong, China.
FAU - Wang, Gongjun
AU  - Wang G
AD  - Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong, China.
FAU - Lv, Jing
AU  - Lv J
AD  - Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong, China.
FAU - Qiu, Wensheng
AU  - Qiu W
AD  - Department of Oncology, The Affiliated Hospital of Qingdao University, Qingdao, 
      Shandong, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210421
PL  - United States
TA  - Aging (Albany NY)
JT  - Aging
JID - 101508617
RN  - 0 (B7-H1 Antigen)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (CD274 protein, human)
RN  - 0 (E2F2 Transcription Factor)
RN  - 0 (PDCD1 protein, human)
RN  - 0 (Programmed Cell Death 1 Receptor)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Aged
MH  - *Autophagy
MH  - B7-H1 Antigen/metabolism
MH  - Biomarkers, Tumor/metabolism
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - DNA Methylation/genetics
MH  - E2F2 Transcription Factor/*antagonists & inhibitors/genetics/metabolism
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Genome, Human
MH  - Humans
MH  - Male
MH  - Multivariate Analysis
MH  - Neoplasm Invasiveness
MH  - Phosphatidylinositol 3-Kinase/*metabolism
MH  - Prognosis
MH  - Programmed Cell Death 1 Receptor/metabolism
MH  - Protein Interaction Maps/genetics
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - *Signal Transduction
MH  - Stomach Neoplasms/*metabolism
MH  - TOR Serine-Threonine Kinases/*metabolism
MH  - Up-Regulation/genetics
PMC - PMC8202834
OTO - NOTNLM
OT  - E2F2
OT  - PI3K/Akt/mTOR pathway
OT  - autophagy
OT  - gastric cancer
OT  - metastasis
COIS- CONFLICTS OF INTEREST: The authors declare that they have no conflicts of 
      interest.
EDAT- 2021/06/07 06:00
MHDA- 2021/07/23 06:00
PMCR- 2021/05/31
CRDT- 2021/06/06 21:07
PHST- 2020/11/24 00:00 [received]
PHST- 2021/03/14 00:00 [accepted]
PHST- 2021/06/06 21:07 [entrez]
PHST- 2021/06/07 06:00 [pubmed]
PHST- 2021/07/23 06:00 [medline]
PHST- 2021/05/31 00:00 [pmc-release]
AID - 202891 [pii]
AID - 10.18632/aging.202891 [doi]
PST - ppublish
SO  - Aging (Albany NY). 2021 Apr 21;13(10):13626-13643. doi: 10.18632/aging.202891. 
      Epub 2021 Apr 21.