Overexpression of lncRNA PTENP1 suppresses glioma cell proliferation and metastasis in vitro.

glioma invasion lncRNA PTENP1 migration proliferation

Journal

OncoTargets and therapy
ISSN: 1178-6930
Titre abrégé: Onco Targets Ther
Pays: New Zealand
ID NLM: 101514322

Informations de publication

Date de publication:
2019
Historique:
entrez: 8 1 2019
pubmed: 8 1 2019
medline: 8 1 2019
Statut: epublish

Résumé

Glioma is one of the most common malignancies of the central nervous system in adults. The lncRNA PTEN pseudogene-1 (PTENP1) has been reported to play an important role in the development and progression of various cancers. However, the molecular mechanism by which lncRNA PTENP1 affects the development and progression of gliomas remains unclear. The levels of PTENP1 expression in glioma tissues and normal brain tissues were detected by quantitative real-time PCR. Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine staining assays were performed to detect cell proliferation. Flow cytometry was used to analyze cell cycle progression. Transwell assay and scratch test were used to detect cell migration and invasion, and Western blot studies were performed to detect protein expression. Our results showed that expression of lncRNA PTENP1 was decreased in glioma tissues when compared with normal brain tissues. Overexpression of PTENP1 suppressed SHG44 and U251 cell proliferation and significantly decreased the numbers of S-phase cells. Furthermore, the invasion and migration abilities of SHG44 and U251 cells were reduced after being transfected with a PTENP1 overexpression plasmid. Overexpression of PTENP1 induced the expression of p21 protein and suppressed the p38 signaling pathway. Our study investigated the function of PTENP1 in glioma and provided new insights for treating that malignancy.

Sections du résumé

BACKGROUND BACKGROUND
Glioma is one of the most common malignancies of the central nervous system in adults. The lncRNA PTEN pseudogene-1 (PTENP1) has been reported to play an important role in the development and progression of various cancers. However, the molecular mechanism by which lncRNA PTENP1 affects the development and progression of gliomas remains unclear.
MATERIALS AND METHODS METHODS
The levels of PTENP1 expression in glioma tissues and normal brain tissues were detected by quantitative real-time PCR. Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine staining assays were performed to detect cell proliferation. Flow cytometry was used to analyze cell cycle progression. Transwell assay and scratch test were used to detect cell migration and invasion, and Western blot studies were performed to detect protein expression.
RESULTS RESULTS
Our results showed that expression of lncRNA PTENP1 was decreased in glioma tissues when compared with normal brain tissues. Overexpression of PTENP1 suppressed SHG44 and U251 cell proliferation and significantly decreased the numbers of S-phase cells. Furthermore, the invasion and migration abilities of SHG44 and U251 cells were reduced after being transfected with a PTENP1 overexpression plasmid. Overexpression of PTENP1 induced the expression of p21 protein and suppressed the p38 signaling pathway.
CONCLUSION CONCLUSIONS
Our study investigated the function of PTENP1 in glioma and provided new insights for treating that malignancy.

Identifiants

pubmed: 30613153
doi: 10.2147/OTT.S182537
pii: ott-12-147
pmc: PMC6306071
doi:

Types de publication

Journal Article

Langues

eng

Pagination

147-156

Déclaration de conflit d'intérêts

Disclosure The authors report no conflicts of interest in this work.

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Auteurs

Su Hu (S)

Department of Neurosurgery, The Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, Guangdong, People's Republic of China, pengbiaopengbiao@msn.com.

Li Xu (L)

Department of Neurosurgery, The Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, Guangdong, People's Republic of China, pengbiaopengbiao@msn.com.
Department of Neurosurgery, The Central People's Hospital of Zhanjiang, Zhanjiang 524045, Guangdong, People's Republic of China.

Lihua Li (L)

Department of Neurosurgery, The Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, Guangdong, People's Republic of China, pengbiaopengbiao@msn.com.

Dongdong Luo (D)

Department of Neurosurgery, The Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, Guangdong, People's Republic of China, pengbiaopengbiao@msn.com.

Hailin Zhao (H)

Department of Neurosurgery, The Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, Guangdong, People's Republic of China, pengbiaopengbiao@msn.com.

Dan Li (D)

Department of Neurosurgery, The Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, Guangdong, People's Republic of China, pengbiaopengbiao@msn.com.

Biao Peng (B)

Department of Neurosurgery, The Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou 510095, Guangdong, People's Republic of China, pengbiaopengbiao@msn.com.

Classifications MeSH