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Gankyrin promotes the proliferation of gastric cancer and is associated with chemosensitivity.

Abstract Although gankyrin is involved in the tumorigenicity and metastasis of some malignancies, the role of gankyrin in gastric cancer is not clear. In this study, we evaluated the function and mechanism of gankyrin in gastric cancer. The effects of gankyrin on gastric cancer growth, proliferation, and chemosensitivity were determined. Gankyrin expression was significantly increased in gastric cancer compared to non-cancerous tissues. This expression significantly enhanced cancer cell proliferation and growth in vitro and in vivo. Suppression of gankyrin downregulated cyclin D1, cyclin E, proliferating cell nuclear antigen, phosphoinositide 3-kinase, AKT, p-PI3K, and p-AKT but upregulated Rb, p53, and p27. However, gankyrin overexpression led to opposite results. Downregulation of gankyrin expression enhanced chemosensitivity to 5-fluorouracil and cisplatin by inducing cell apoptosis. However, upregulation of gankyrin expression led to the opposite outcomes. Gankyrin enhanced gastric cancer cell proliferation by regulating cell cycle-related proteins and by activating PI3K/AKT signaling pathway. Gankyrin played an important role in gastric carcinogenesis and could be a potential effective therapeutic target for enhancing chemosensitivity to 5-fluorouracil and cisplatin.
PMID
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Authors

Mayor MeshTerms
Keywords

Gankyrin

cell cycle

chemosensitivity

gastric cancer

small interfering RNA

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




PMID- 28653901
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  - Gankyrin promotes the proliferation of gastric cancer and is associated with
      chemosensitivity.
PG  - 1010428317704820
LID - 10.1177/1010428317704820 [doi]
AB  - Although gankyrin is involved in the tumorigenicity and metastasis of some
      malignancies, the role of gankyrin in gastric cancer is not clear. In this study,
      we evaluated the function and mechanism of gankyrin in gastric cancer. The
      effects of gankyrin on gastric cancer growth, proliferation, and chemosensitivity
      were determined. Gankyrin expression was significantly increased in gastric
      cancer compared to non-cancerous tissues. This expression significantly enhanced 
      cancer cell proliferation and growth in vitro and in vivo. Suppression of
      gankyrin downregulated cyclin D1, cyclin E, proliferating cell nuclear antigen,
      phosphoinositide 3-kinase, AKT, p-PI3K, and p-AKT but upregulated Rb, p53, and
      p27. However, gankyrin overexpression led to opposite results. Downregulation of 
      gankyrin expression enhanced chemosensitivity to 5-fluorouracil and cisplatin by 
      inducing cell apoptosis. However, upregulation of gankyrin expression led to the 
      opposite outcomes. Gankyrin enhanced gastric cancer cell proliferation by
      regulating cell cycle-related proteins and by activating PI3K/AKT signaling
      pathway. Gankyrin played an important role in gastric carcinogenesis and could be
      a potential effective therapeutic target for enhancing chemosensitivity to
      5-fluorouracil and cisplatin.
FAU - Zeng, Yue-Can
AU  - Zeng YC
AD  - The Fourth Laboratory of Cancer Institute, Department of Tumor Pathology of
      General Surgery Institute, The First Affiliated Hospital of China Medical
      University, Shenyang, China.
FAU - Sun, Dan
AU  - Sun D
AD  - The Fourth Laboratory of Cancer Institute, Department of Tumor Pathology of
      General Surgery Institute, The First Affiliated Hospital of China Medical
      University, Shenyang, China.
FAU - Li, Wen-Hui
AU  - Li WH
AD  - The Fourth Laboratory of Cancer Institute, Department of Tumor Pathology of
      General Surgery Institute, The First Affiliated Hospital of China Medical
      University, Shenyang, China.
FAU - Zhao, Jing
AU  - Zhao J
AD  - The Fourth Laboratory of Cancer Institute, Department of Tumor Pathology of
      General Surgery Institute, The First Affiliated Hospital of China Medical
      University, Shenyang, China.
FAU - Xin, Yan
AU  - Xin Y
AD  - The Fourth Laboratory of Cancer Institute, Department of Tumor Pathology of
      General Surgery Institute, The First Affiliated Hospital of China Medical
      University, Shenyang, 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 (Neoplasm Proteins)
RN  - 0 (PSMD10 protein, human)
RN  - 0 (Proto-Oncogene Proteins)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Oncogene Protein v-akt)
RN  - EC 3.4.25.1 (Proteasome Endopeptidase Complex)
RN  - Q20Q21Q62J (Cisplatin)
RN  - U3P01618RT (Fluorouracil)
SB  - IM
MH  - Apoptosis/drug effects/genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Cisplatin/administration & dosage
MH  - Drug Resistance, Neoplasm/*genetics
MH  - Fluorouracil/administration & dosage
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Neoplasm Proteins/biosynthesis/genetics
MH  - Oncogene Protein v-akt/genetics
MH  - Phosphatidylinositol 3-Kinases/genetics
MH  - Proteasome Endopeptidase Complex/*biosynthesis/genetics
MH  - Proto-Oncogene Proteins/*biosynthesis/genetics
MH  - Signal Transduction/drug effects
MH  - Stomach Neoplasms/*drug therapy/*genetics/pathology
OTO - NOTNLM
OT  - Gankyrin
OT  - cell cycle
OT  - chemosensitivity
OT  - gastric cancer
OT  - small interfering RNA
EDAT- 2017/06/28 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/28 06:00
AID - 10.1177/1010428317704820 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317704820. doi: 10.1177/1010428317704820.