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Sirtuin 6 plays an oncogenic role and induces cell autophagy in esophageal cancer cells.

Abstract Sirtuin 6, a member of sirtuin family, is generally regarded as a tumor suppressor as it participates in suppressing hypoxia-inducible factor 1α and MYC transcription activity by deacetylating H3K9 (histone H3 lysine 9) and H3K56 (histone H3 lysine) at promoters of target genes, leading to the aerobic glycolysis inhibition and cell growth suppression. However, its expression has recently been reported to be highly elevated in a series of tumors, including prostate cancer, breast cancer, and non-small cell lung cancer, indicating that sirtuin 6 plays dual roles in tumorigenicity in a cell/tumor type-specific manner. To our knowledge, the biological roles of sirtuin 6 in esophageal cancer cells have still been underestimated. In the study, data from quantitative reverse transcriptase polymerase chain reaction-based assays and immunohistochemical assays revealed that sirtuin 6 was remarkably overexpressed in esophageal squamous tumor tissues. Moreover, its upregulation was closely related with clinical features, such as gender, pathology, tumor-node-metastasis, and cell differentiation. Subsequently, the biological tests showed that it promoted cell proliferation and induced the expression of Bcl2, a key anti-apoptotic factor, in esophageal carcinoma cells. Moreover, using the ratio of LC3II/I, a widely recognized autophagy biomarker, we showed that it apparently induced cell autophagy, which was further confirmed by the autophagy flux assays. In addition, results from western blotting assays and immunoprecipitation assays displayed that sirtuin 6 specifically interacted with ULK1 and positively regulated its activity by inhibiting its upstream factor mammalian target of rapamycin activity. In summary, our studies shed insights into the crucial functions of sirtuin 6 in esophageal carcinoma cells and provide evidence supporting sirtuin 6-based personalized therapies in esophageal carcinoma cell patients.
PMID
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Authors

Mayor MeshTerms
Keywords

Sirtuin 6

ULK1

autophagy

cell growth

mammalian target of rapamycin

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28653878
OWN - NLM
STAT- MEDLINE
DA  - 20170627
DCOM- 20170711
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Sirtuin 6 plays an oncogenic role and induces cell autophagy in esophageal cancer
      cells.
PG  - 1010428317708532
LID - 10.1177/1010428317708532 [doi]
AB  - Sirtuin 6, a member of sirtuin family, is generally regarded as a tumor
      suppressor as it participates in suppressing hypoxia-inducible factor 1alpha and 
      MYC transcription activity by deacetylating H3K9 (histone H3 lysine 9) and H3K56 
      (histone H3 lysine) at promoters of target genes, leading to the aerobic
      glycolysis inhibition and cell growth suppression. However, its expression has
      recently been reported to be highly elevated in a series of tumors, including
      prostate cancer, breast cancer, and non-small cell lung cancer, indicating that
      sirtuin 6 plays dual roles in tumorigenicity in a cell/tumor type-specific
      manner. To our knowledge, the biological roles of sirtuin 6 in esophageal cancer 
      cells have still been underestimated. In the study, data from quantitative
      reverse transcriptase polymerase chain reaction-based assays and
      immunohistochemical assays revealed that sirtuin 6 was remarkably overexpressed
      in esophageal squamous tumor tissues. Moreover, its upregulation was closely
      related with clinical features, such as gender, pathology, tumor-node-metastasis,
      and cell differentiation. Subsequently, the biological tests showed that it
      promoted cell proliferation and induced the expression of Bcl2, a key
      anti-apoptotic factor, in esophageal carcinoma cells. Moreover, using the ratio
      of LC3II/I, a widely recognized autophagy biomarker, we showed that it apparently
      induced cell autophagy, which was further confirmed by the autophagy flux assays.
      In addition, results from western blotting assays and immunoprecipitation assays 
      displayed that sirtuin 6 specifically interacted with ULK1 and positively
      regulated its activity by inhibiting its upstream factor mammalian target of
      rapamycin activity. In summary, our studies shed insights into the crucial
      functions of sirtuin 6 in esophageal carcinoma cells and provide evidence
      supporting sirtuin 6-based personalized therapies in esophageal carcinoma cell
      patients.
FAU - Huang, Nan
AU  - Huang N
AD  - 1 Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of
      Tongji University, Shanghai, China.
FAU - Liu, Zhiwei
AU  - Liu Z
AD  - 2 Department of Laboratory, Central Hospital of Panyu District, Guangzhou, China.
FAU - Zhu, Jiabei
AU  - Zhu J
AD  - 3 Department of Laboratory Medicine, Shanghai Children's Medical Center, Shanghai
      Jiao Tong University School of Medicine, Shanghai, China.
FAU - Cui, Zhongqi
AU  - Cui Z
AD  - 1 Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of
      Tongji University, Shanghai, China.
FAU - Li, Yuguang
AU  - Li Y
AD  - 2 Department of Laboratory, Central Hospital of Panyu District, Guangzhou, China.
FAU - Yu, Yongchun
AU  - Yu Y
AD  - 4 Central Laboratory, Shanghai Municipal Hospital of Traditional Chinese Medicine
      Affiliated With Shanghai TCM University, Shanghai, China.
FAU - Sun, Fenyong
AU  - Sun F
AD  - 1 Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of
      Tongji University, Shanghai, China.
FAU - Pan, Qiuhui
AU  - Pan Q
AD  - 3 Department of Laboratory Medicine, Shanghai Children's Medical Center, Shanghai
      Jiao Tong University School of Medicine, Shanghai, China.
FAU - Yang, Qingyuan
AU  - Yang Q
AD  - 1 Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of
      Tongji University, Shanghai, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - EC 2.7.11.1 (Autophagy-Related Protein-1 Homolog)
RN  - EC 2.7.11.1 (ULK1 protein, human)
RN  - EC 3.5.1.- (SIRT6 protein, human)
RN  - EC 3.5.1.- (Sirtuins)
RN  - W36ZG6FT64 (Sirolimus)
SB  - IM
MH  - Apoptosis/genetics
MH  - Autophagy/genetics
MH  - Autophagy-Related Protein-1 Homolog/biosynthesis/*genetics
MH  - Biomarkers, Tumor/biosynthesis/*genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation/genetics
MH  - Esophageal Neoplasms/*genetics/pathology
MH  - Gene Expression Regulation, Neoplastic
MH  - Glycolysis/genetics
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins/biosynthesis/*genetics
MH  - Sirolimus/administration & dosage
MH  - Sirtuins/biosynthesis/*genetics
OTO - NOTNLM
OT  - Sirtuin 6
OT  - ULK1
OT  - autophagy
OT  - cell growth
OT  - mammalian target of rapamycin
EDAT- 2017/06/28 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/28 06:00
AID - 10.1177/1010428317708532 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317708532. doi: 10.1177/1010428317708532.