PMID- 27807322
OWN - NLM
STAT- MEDLINE
DCOM- 20171128
LR  - 20211204
IS  - 1672-7347 (Print)
IS  - 1672-7347 (Linking)
VI  - 41
IP  - 10
DP  - 2016 Oct 28
TI  - [Influence of HMGB1/MAPK/m-TOR signaling pathway on cell autophagy and 
      chemotherapy resistance in K562 cells].
PG  - 1016-1023
AB  - To observe the effect of high-mobility group box 1 (HMGB1) on autophagy and 
      chemotherapy resistance in human leukemiacell line (K562) cells, and to explore 
      the underlying mechanisms.
 Methods: The K562 cells were cultured in vitro and 
      divided into 6 groups: a chemotherapeutic group, a chemotherapeutic control 
      group, a HMGB1 preconditioning group, a HMGB1 preconditioning control group, a 
      HMGB1 siRNA group and a siRNA control group. The chemotherapeutic group was 
      further divided into a vincristine (VCR) group, an etoposide (VP-16) group, a 
      cytosine arabinoside (Ara-C) group, a adriamycin (ADM) group and a arsenic 
      trioxide (As2O3) group. The cell activity was evaluated by cell counting kit-8. 
      The protein levels of HMGB1, microtubule-associate protein1light chain3 (LC3), 
      AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (m-TOR) 
      were determined by Western blotting. The level of serum HMGB1 was evaluated by 
      enzyme-linked immunosorbent assay (ELISA). The autophagy was examined by 
      monodansylcadaverine staining and observed under transmission electron 
      microscopy.
 Results: Compared with the control group, the cell activity was 
      significantly decreased and the level of serum HMGB1 was significantly increased 
      in the chemotherapeutic (VCR, VP-16, Ara-C, ADM and As2O3) groups (all P<0.05). 
      Compared with the control group, the cell activity and the level of serum HMGB1 
      were significantly increased in the HMGB1 preconditioning group (both P<0.05). 
      Compared with the siRNA control group, the cell activity and the level of serum 
      HMGB1 were significantly decreased in the HMGB1 siRNA group (both P<0.05). 
      Compared with the control group, the expression of LC3-II and the formation of 
      autophagic bodies were increased in the HMGB1 preconditioning group (both 
      P<0.05), the p-AMPK expression was increased and p-mTOR expression was decreased 
      (both P<0.05).
 Conclusion: HMGB1 can increase the autophagy and promote 
      chemotherapy resistance through the pathway of AMPK/m-TOR in K562 cells.
FAU - Liu, Liying
AU  - Liu L
AD  - Department of Pediatrics, Shandong Provincial Hospital Affiliated to Shangdong 
      University, Jinan 250021, China.
FAU - Gao, Fei
AU  - Gao F
AD  - Department of Pediatrics, Shandong Provincial Hospital Affiliated to Shangdong 
      University, Jinan 250021, China.
FAU - Ye, Yanqiong
AU  - Ye Y
AD  - Department of Cardiac Surgery, Guangdong General Hospital, Guangzhou 510010, 
      China.
FAU - Chen, Zhiheng
AU  - Chen Z
AD  - Department of Pediatrics, Third Xiangya Hospital, Central South University, 
      Changsha 410013, China.
FAU - Dai, Yunpeng
AU  - Dai Y
AD  - Department of Pediatrics, Shandong Provincial Hospital Affiliated to Shangdong 
      University, Jinan 250021, China.
FAU - Zhao, Ping
AU  - Zhao P
AD  - Department of Pediatrics, Shandong Provincial Hospital Affiliated to Shangdong 
      University, Jinan 250021, China.
FAU - Guan, Guotao
AU  - Guan G
AD  - Department of Pediatrics, Shandong Provincial Hospital Affiliated to Shangdong 
      University, Jinan 250021, China.
FAU - Zhao, Mingyi
AU  - Zhao M
AD  - Department of Pediatrics, Third Xiangya Hospital, Central South University, 
      Changsha 410013, China.
LA  - chi
PT  - Journal Article
PL  - China
TA  - Zhong Nan Da Xue Xue Bao Yi Xue Ban
JT  - Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. 
      Medical sciences
JID - 101230586
RN  - 0 (Arsenicals)
RN  - 0 (HMGB1 Protein)
RN  - 0 (MAP1LC3A protein, human)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Oxides)
RN  - 0 (RNA, Small Interfering)
RN  - 04079A1RDZ (Cytarabine)
RN  - 5J49Q6B70F (Vincristine)
RN  - 6PLQ3CP4P3 (Etoposide)
RN  - 80168379AG (Doxorubicin)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - S7V92P67HO (Arsenic Trioxide)
SB  - IM
MH  - AMP-Activated Protein Kinases/*genetics/*physiology
MH  - Arsenic Trioxide
MH  - Arsenicals
MH  - Autophagy/*genetics
MH  - Cytarabine
MH  - Doxorubicin
MH  - Drug Resistance, Neoplasm/*genetics/*physiology
MH  - Etoposide
MH  - HMGB1 Protein/*genetics/*physiology
MH  - Humans
MH  - K562 Cells/physiology
MH  - Microtubule-Associated Proteins
MH  - Oxides
MH  - RNA, Small Interfering
MH  - Signal Transduction
MH  - TOR Serine-Threonine Kinases/*genetics/*physiology
MH  - Vincristine
EDAT- 2016/11/04 06:00
MHDA- 2017/11/29 06:00
CRDT- 2016/11/04 06:00
PHST- 2016/11/04 06:00 [pubmed]
PHST- 2017/11/29 06:00 [medline]
PHST- 2016/11/04 06:00 [entrez]
AID - 10.11817/j.issn.1672-7347.2016.10.002 [doi]
PST - ppublish
SO  - Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2016 Oct 28;41(10):1016-1023. doi: 
      10.11817/j.issn.1672-7347.2016.10.002.