PMID- 34488535
OWN - NLM
STAT- MEDLINE
DCOM- 20211217
LR  - 20220204
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 12
IP  - 1
DP  - 2021 Dec
TI  - Liquiritigenin exerts the anti-cancer role in oral cancer via inducing 
      autophagy-related apoptosis through PI3K/AKT/mTOR pathway inhibition in vitro and 
      in vivo.
PG  - 6070-6082
LID - 10.1080/21655979.2021.1971501 [doi]
AB  - Operative treatment on oral cancer greatly damages the chewing and language 
      function of the patient, we aim to find better solution with fewer side effects. 
      The anti-tumor effects of Liquiritigenin (LQ) have been explored in kinds of 
      cancers, but not in oral cancer. In this study, our purpose is to reveal the 
      effects of LQ on oral cancer and the associated mechanism.Cell proliferation was 
      examined through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide 
      (MTT) assay and 5-Ethynyl-2'- deoxyuridine (EDU) staining. Cell apoptosis in 
      cells and tissues were assessed by flow cytometry and terminal dexynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) staining, respectively. 
      Expressions of AKT and light chain 3 (LC3) were detected through 
      Immunofluorescence. In addition, xenograft model was established by injecting the 
      CAL-27 cells (2 x 10(6)) subcutaneously into the right flanks of mice. Expression 
      of Ki67 and Beclin1 in tissues was valued by Immunohistochemistry (IHC).We found 
      that cell viability of CAL-27 and SCC-9 was effectively inhibited by LQ. Besides, 
      obvious cell apoptosis and cell autophagy were induced by LQ. In addition, 
      PI3K/AKT/mTOR pathway was sharply inactivated by LQ in oral cancer cells. 
      Corresponding in vivo experiments demonstrated that tumor growth was largely 
      restricted, cell apoptosis was augmented and autophagy was enhanced by LQ. What 
      is more, phosphorylation of AKT in tumor tissues could also be inhibited by LQ. 
      LQ inhibited the progression of oral cancer through inducing autophagy-associated 
      apoptosis via PI3K/AKT/mTOR pathway inhibition, revealing a new possible scheme 
      for the treatment of oral cancer.
FAU - Ji, Yingchen
AU  - Ji Y
AD  - Department of Stomatology, Jiangsu Provincial Hospital of Traditional Chinese 
      Medicine, Jiangsu, 210029, China.
FAU - Hu, Weiwei
AU  - Hu W
AD  - Department of Stomatology, Huai'an Second People's Hospital and Affiliated 
      Huai'an Hospital of Xuzhou Medical University, Jiangsu, China.
FAU - Jin, Yan
AU  - Jin Y
AD  - Department of Medical Oncology, Affiliated Huai'an No.1 People's Hospital, 
      Nanjing Medical University, Jiangsu, China.
FAU - Yu, Huiming
AU  - Yu H
AD  - Department of Stomatology, Jiangsu Provincial Hospital of Traditional Chinese 
      Medicine, Jiangsu, 210029, China.
FAU - Fang, Jin
AU  - Fang J
AD  - Department of Stomatology, Affiliated Huai'an No.1 People's Hospital, Nanjing 
      Medical University, Jiangsu, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Flavanones)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - T194LKP9W6 (liquiritigenin)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents/*pharmacology
MH  - Apoptosis/drug effects
MH  - Autophagy/*drug effects
MH  - Cell Line, Tumor
MH  - Female
MH  - Flavanones/*pharmacology
MH  - Humans
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mouth Neoplasms/*metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Signal Transduction/*drug effects
MH  - TOR Serine-Threonine Kinases/metabolism
PMC - PMC8806794
OTO - NOTNLM
OT  - Autophagy
OT  - apoptosis
OT  - oncology
OT  - oral cancer
OT  - signal pathway
OT  - traditional chinese medicine
COIS- The authors have declared that no competing interest exists.
EDAT- 2021/09/08 06:00
MHDA- 2021/12/18 06:00
PMCR- 2021/09/07
CRDT- 2021/09/07 05:48
PHST- 2021/09/07 05:48 [entrez]
PHST- 2021/09/08 06:00 [pubmed]
PHST- 2021/12/18 06:00 [medline]
PHST- 2021/09/07 00:00 [pmc-release]
AID - 1971501 [pii]
AID - 10.1080/21655979.2021.1971501 [doi]
PST - ppublish
SO  - Bioengineered. 2021 Dec;12(1):6070-6082. doi: 10.1080/21655979.2021.1971501.