PMID- 31938256
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200325
IS  - 1936-2625 (Electronic)
IS  - 1936-2625 (Linking)
VI  - 11
IP  - 3
DP  - 2018
TI  - Influence of SIRT6 regulation of cellular glycometabolism on radiosensitivity of 
      non-small-cell lung cancer A549 cells.
PG  - 1575-1580
AB  - OBJECTIVE: To investigate the influence of SIRT6 mediated regulation of cellular 
      glycometabolism on radiosensitivity of A549 non-small-cell lung cancer (NSCLC) 
      cells. METHODS: Ad-SIRT6 adenovirus vector overexpressed SIRT6 and was 
      established and divided into a control group, a zero-load group (Ad-null), and an 
      overexpression group (Ad-SIRT6). The virus concentration of the Ad-null group and 
      the Ad-SIRT6 group was 200 pfu/cell. The survival factor (SF) after X-ray 
      irradiation of 0, 2, 4, 6, 8, and 10 Gy in three groups was detected by clone 
      formation and cell cycle and apoptosis after 4 Gy X-ray irradiation for 48 hours 
      in the three groups was detected by flow cytometry. Expression levels of pyruvate 
      kinase (PKM), lactate dehydrogenase (LDHA), and hexokinase (HK) after 4 Gy X-ray 
      irradiation of 48 h were detected by qPCR. The glucose level after consumption of 
      (1x10(6)) cells in the medium was detected by a glucose kit. RESULTS: Compared 
      with the control group and the Ad-null group, SFs after X-ray irradiation of 4-10 
      Gy in the Ad-SIRT6 group were decreased (P<0.05). A sensitization enhancement 
      ratio of the Ad-SIRT group/the control group was 1.451. After 4 Gy X-ray 
      irradiation of 48 h, the cell ratio and apoptosis rate in G(1) phase were 
      increased in the Ad-SIRT6 group, with statistical significance when compared with 
      the other two groups (P<0.05). Compared with the control group and the Ad-null 
      group, levels of PKM, LDHA, and HK mRNA in Ad-SIRT6 group were decreased (P<0.05) 
      and the remaining glucose in the medium was increased (P<0.05). CONCLUSION: 
      Overexpression of SIRT6 can inhibit key-enzyme generation in A549 cells to 
      inhibit glycolysis, enhance the radiosensitivity, and lead to G(0)/G(1) phase 
      block as well as cell apoptosis.
CI  - IJCEP Copyright (c) 2018.
FAU - Cai, Yong
AU  - Cai Y
AD  - Department of Radiation Oncology, Shanghai Pulmonary Hospital, Tongji University 
      School of Medicine Shanghai, China.
FAU - Sheng, Zhaoying
AU  - Sheng Z
AD  - Department of Radiation Oncology, Shanghai Pulmonary Hospital, Tongji University 
      School of Medicine Shanghai, China.
FAU - Chen, Yun
AU  - Chen Y
AD  - Department of Radiation Oncology, Shanghai Pulmonary Hospital, Tongji University 
      School of Medicine Shanghai, China.
FAU - Wang, Jiying
AU  - Wang J
AD  - Department of Oncology, Shanghai Pulmonary Hospital, Tongji University School of 
      Medicine Shanghai, China.
LA  - eng
PT  - Journal Article
DEP - 20180301
PL  - United States
TA  - Int J Clin Exp Pathol
JT  - International journal of clinical and experimental pathology
JID - 101480565
PMC - PMC6958171
OTO - NOTNLM
OT  - SIRT6
OT  - glycolysis
OT  - non-small-cell lung cancer
OT  - radiosensitivity
COIS- None.
EDAT- 2018/03/01 00:00
MHDA- 2018/03/01 00:01
PMCR- 2018/03/01
CRDT- 2020/01/16 06:00
PHST- 2017/12/10 00:00 [received]
PHST- 2017/12/28 00:00 [accepted]
PHST- 2020/01/16 06:00 [entrez]
PHST- 2018/03/01 00:00 [pubmed]
PHST- 2018/03/01 00:01 [medline]
PHST- 2018/03/01 00:00 [pmc-release]
PST - epublish
SO  - Int J Clin Exp Pathol. 2018 Mar 1;11(3):1575-1580. eCollection 2018.