Silencing of MAP4K4 by short hairpin RNA suppresses proliferation, induces G1 cell cycle arrest and induces apoptosis in gastric cancer cells

Autor: Yun‑Min Lu, Yuan‑Fei Liu, Yuan Liu, Xiao‑Hong Liao, Wu‑Ming Kong, Guo‑Qiang Qu, Wei-Xiong Chen
Jazyk: angličtina
Rok vydání: 2015
Předmět:
0301 basic medicine
Male
Cancer Research
Apoptosis
Biochemistry
Small hairpin RNA
0302 clinical medicine
RNA interference
RNA
Small Interfering

Notch signaling
bcl-2-Associated X Protein
Aged
80 and over

biology
Receptors
Notch

Intracellular Signaling Peptides and Proteins
Articles
Cell cycle
Middle Aged
Cell biology
Gene Expression Regulation
Neoplastic

Oncology
030220 oncology & carcinogenesis
Gene Knockdown Techniques
Molecular Medicine
Female
RNA Interference
Signal transduction
Signal Transduction
Adult
Down-Regulation
Protein Serine-Threonine Kinases
03 medical and health sciences
Bcl-2-associated X protein
Stomach Neoplasms
Cell Line
Tumor

Genetics
Humans
Neoplasm Invasiveness
Gene Silencing
RNA
Messenger

Protein kinase A
Molecular Biology
Aged
Cell Proliferation
G1 arrest
Cell growth
gastric cancer
G1 Phase Cell Cycle Checkpoints
030104 developmental biology
Cancer cell
biology.protein
Cancer research
MAP4K4
Zdroj: Molecular Medicine Reports
ISSN: 1791-3004
1791-2997
Popis: Gastric cancer (GC) is the second most common cause of cancer-associated mortality worldwide. Previous studies suggest that mitogen-activated protein kinase kinase kinase kinase isoform 4 (MAP4K4) is involved in cancer cell growth, apoptosis and migration. In the present study, bioinformatics analysis and reverse transcription-quantitative polymerase chain reaction were performed to determine if MAP4K4 was overexpressed in GC. The knockdown of MAP4K4 by RNA interference in GC cells markedly inhibited cell proliferation, which may be mediated by cell cycle arrest in the G1 phase. The silencing of MAP4K4 also induced cell apoptosis by increasing the ratio of Bax/Bcl-2. In addition, Notch signaling was markedly reduced by MAP4K4 silencing. The results of the present study suggested that inhibition of MAP4K4 may be a therapeutic strategy for GC.
Databáze: OpenAIRE