PMID- 36683349
OWN - NLM
STAT- MEDLINE
DCOM- 20230511
LR  - 20230511
IS  - 1099-0461 (Electronic)
IS  - 1095-6670 (Linking)
VI  - 37
IP  - 5
DP  - 2023 May
TI  - Dieckol, a natural polyphenolic drug, inhibits the proliferation and migration of 
      colon cancer cells by inhibiting PI3K, AKT, and mTOR phosphorylation.
PG  - e23313
LID - 10.1002/jbt.23313 [doi]
AB  - This study investigated that dieckol (DKL), a natural drug, inhibits colon cancer 
      cell proliferation and migration by inhibiting phosphoinositide-3-kinase (PI3K), 
      protein kinase B (AKT), and mammalian target of rapamycin (mTOR) phosphorylation 
      in HCT-116 cells. The cells were treated with DKL in various concentrations (32 
      and 50 muM) for 24 h and then analyzed for various experiments. MTT (tetrazolium 
      bromide) and crystal violet assay investigated DKL-mediated cytotoxicity. 
      Dichlorodihydrofluorescein diacetate staining was used to assess the reactive 
      oxygen species (ROS) measurement, and apoptotic changes were studied by dual 
      acridine orange and ethidium bromide staining. Protein expression of cell 
      survival, cell cycle, proliferation, and apoptosis protein was evaluated by 
      western blot analysis. Results indicated that DKL produces significant 
      cytotoxicity in HCT-116, and the half-maximal inhibitory concentration was found 
      to be 32 muM for 24-h incubation. Moreover, effective production of ROS and 
      enhanced apoptotic signs were observed upon DKL treatment in HCT-116. DKL induces 
      the expression of phosphorylated PI3K, AKT, and mToR-associated enhanced 
      expression of cyclin-D1, proliferating cell nuclear antigen, cyclin-dependent 
      kinase (CDK)-4, CDK-6, and Bcl-2 in HCT-116. In addition, proapoptotic proteins 
      such as Bax, caspase-9, and caspase-3 were significantly enhanced by DKL 
      treatment in HCT-116. Hence, DKL has been considered a chemotherapeutic drug by 
      impeding the expression of PI3K-, AKT-, and mTOR-mediated inhibition of 
      proliferation and cell cycle-regulating proteins.
CI  - (c) 2023 Wiley Periodicals LLC.
FAU - Dai, Wei
AU  - Dai W
AD  - Department of Clinical Laboratory, Ganzhou People's Hospital, Jiangxi, Ganzhou, 
      China.
FAU - Dai, Yong Gang
AU  - Dai YG
AD  - Department of Clinical Laboratory, Shandong Provincial Third Hospital, Jinan, 
      Shandong, China.
FAU - Ren, Dong Feng
AU  - Ren DF
AD  - Department of Oncology, The First Hospital of Yulin, Shaanxi, Yulin, China.
FAU - Zhu, Da Wei
AU  - Zhu DW
AUID- ORCID: 0000-0001-8476-0397
AD  - Department of Gastroenterology, Hongze District People's Hospital, Jiangsu, 
      Huai'an, China.
LA  - eng
PT  - Journal Article
DEP - 20230122
PL  - United States
TA  - J Biochem Mol Toxicol
JT  - Journal of biochemical and molecular toxicology
JID - 9717231
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - 0 (dieckol)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.1.1 (MTOR protein, human)
SB  - IM
MH  - Humans
MH  - Phosphorylation
MH  - *Phosphatidylinositol 3-Kinase
MH  - Proto-Oncogene Proteins c-akt
MH  - Phosphatidylinositol 3-Kinases
MH  - Reactive Oxygen Species
MH  - *Colonic Neoplasms/drug therapy
MH  - TOR Serine-Threonine Kinases
MH  - Cell Proliferation
OTO - NOTNLM
OT  - PI3K/AKT/mTOR
OT  - apoptosis
OT  - colon cancer
OT  - dieckol
OT  - proliferation
EDAT- 2023/01/24 06:00
MHDA- 2023/05/11 06:42
CRDT- 2023/01/23 02:03
PHST- 2022/12/07 00:00 [revised]
PHST- 2022/09/01 00:00 [received]
PHST- 2023/01/05 00:00 [accepted]
PHST- 2023/05/11 06:42 [medline]
PHST- 2023/01/24 06:00 [pubmed]
PHST- 2023/01/23 02:03 [entrez]
AID - 10.1002/jbt.23313 [doi]
PST - ppublish
SO  - J Biochem Mol Toxicol. 2023 May;37(5):e23313. doi: 10.1002/jbt.23313. Epub 2023 
      Jan 22.