PMID- 32982778
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 11
DP  - 2020
TI  - Cucurbitacin E Induces Autophagy-Involved Apoptosis in Intestinal Epithelial 
      Cells.
PG  - 1020
LID - 10.3389/fphys.2020.01020 [doi]
LID - 1020
AB  - Apoptosis plays a crucial role in maintaining the structural and functional 
      integrity of the intestinal epithelial barrier. Autophagy mediates injury to and 
      repair of the intestinal epithelial barrier through multiple pathways in 
      pathophysiological conditions. Our earlier study has found that cucurbitacin E 
      (CuE) regulates the proliferation, migration, and permeability of human 
      intestinal epithelial cells (IECs); however, its effects and mechanisms on 
      apoptosis and autophagy are still unclear. This study reported CuE induced 
      apoptosis and promoted autophagy of IECs in a concentration-dependent manner. The 
      results showed that CuE could inhibit the expression of apoptosis-related protein 
      Bcl-2 and drove activation of caspase-3 and cleavage of its substrate poly 
      (ADP-ribose) polymerase. CuE also facilitated the expression of endoplasmic 
      reticulum stress-related proteins, CHOP and Grp78, and autophagy-related 
      proteins, Beclin1 and LC3, while inhibiting the phosphorylation of AKT and 
      mammalian target of rapamycin (mTOR). An autophagy inhibitor, 3-methyladenine, 
      reduced CuE-induced apoptosis. These results suggest that CuE may induce 
      apoptosis and autophagy in IECs via the PI3K/AKT/mTOR signaling pathway and that 
      autophagy following endoplasmic reticulum stress participates in the 
      pro-apoptotic process induced by CuE.
CI  - Copyright (c) 2020 Song, Sui, Zhang, Wang and Wang.
FAU - Song, Huapei
AU  - Song H
AD  - State Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn 
      Research, Southwest Hospital, Third Military Medical University (Army Medical 
      University), Chongqing, China.
FAU - Sui, Hehuan
AU  - Sui H
AD  - State Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn 
      Research, Southwest Hospital, Third Military Medical University (Army Medical 
      University), Chongqing, China.
AD  - Department of Pharmacy, Central Hospital of Nanchong, The Second Clinical School 
      of North Sichuan Medical College, Nanchong, China.
AD  - Nanchong Key Laboratory of Individualized Drug Therapy, Nanchong, China.
FAU - Zhang, Qiong
AU  - Zhang Q
AD  - State Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn 
      Research, Southwest Hospital, Third Military Medical University (Army Medical 
      University), Chongqing, China.
FAU - Wang, Pei
AU  - Wang P
AD  - State Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn 
      Research, Southwest Hospital, Third Military Medical University (Army Medical 
      University), Chongqing, China.
FAU - Wang, Fengjun
AU  - Wang F
AD  - State Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn 
      Research, Southwest Hospital, Third Military Medical University (Army Medical 
      University), Chongqing, China.
LA  - eng
PT  - Journal Article
DEP - 20200826
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC7479753
OTO - NOTNLM
OT  - apoptosis
OT  - autophagy
OT  - cucurbitacin E
OT  - endoplasmic reticulum stress
OT  - intestinal epithelial cells
EDAT- 2020/09/29 06:00
MHDA- 2020/09/29 06:01
PMCR- 2020/08/26
CRDT- 2020/09/28 05:39
PHST- 2020/04/30 00:00 [received]
PHST- 2020/07/27 00:00 [accepted]
PHST- 2020/09/28 05:39 [entrez]
PHST- 2020/09/29 06:00 [pubmed]
PHST- 2020/09/29 06:01 [medline]
PHST- 2020/08/26 00:00 [pmc-release]
AID - 10.3389/fphys.2020.01020 [doi]
PST - epublish
SO  - Front Physiol. 2020 Aug 26;11:1020. doi: 10.3389/fphys.2020.01020. eCollection 
      2020.