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Long Non-Coding RNA (lncRNA) Growth Arrest Specific 5 (GAS5) Suppresses Esophageal Squamous Cell Carcinoma Cell Proliferation and Migration by Inactivating Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway.
Med Sci Monit 2018; 24:7689-7696MS

Abstract

BACKGROUND

lncRNA GAS5 acts as a tumor-suppressor gene in various types of malignancies, but its involvement in esophageal cancer has not been well studied. MATERIAL AND

METHODS

A total of 112 patients with esophageal cancer and 55 volunteers with normal physiological conditions were included in this study. Tumor tissues and adjacent healthy tissues were collected from esophageal cancer patients and blood was extracted from patients and controls. Expression of GAS5 in those tissues was detected by qRT-PCR. All patients were followed up for 5 years and diagnostic and prognostic values of serum GAS5 for esophageal cancer were investigated by ROC curve analysis and survival curve analysis, respectively. Effects of GAS5 expression on cell proliferation and migration were investigated by CCK-8 assay and Transwell cell migration assay, respectively. Effects of GAS5 overexpression on expression of PI3K/AKT/mTOR-related proteins were explored by Western blot analysis.

RESULTS

GAS5 expression level was lower in tumor tissues than in adjacent healthy tissues. Serum level of GAS5 was lower in cancer patients than in healthy controls, and serum level of GAS5 was decreased with increase in stage of primary tumor (T stage). GAS5 overexpression inhibited tumor cell proliferation and migration, while treatment with PI3K activator reduced the inhibitory effects. GAS5 overexpression decreased the expression level of PI3K and phosphorylation levels of Akt and mTOR in esophageal cancer cells, while PI3K activator treatment showed no significant effects on GAS5 expression.

CONCLUSIONS

GAS5 was downregulated in esophageal cancer patients compared to healthy controls, and GAS5 overexpression suppressed proliferation and migration of esophageal cancer cells by inactivating the PI3K/AKT/mTOR pathway.

Authors+Show Affiliations

Department of Gastrointestinal Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).Department of Gastrointestinal Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).Department of Gastrointestinal Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).Department of Gastrointestinal Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China (mainland).

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30368517

Citation

Wang, Guojun, et al. "Long Non-Coding RNA (lncRNA) Growth Arrest Specific 5 (GAS5) Suppresses Esophageal Squamous Cell Carcinoma Cell Proliferation and Migration By Inactivating Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway." Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, vol. 24, 2018, pp. 7689-7696.
Wang G, Sun J, Zhao H, et al. Long Non-Coding RNA (lncRNA) Growth Arrest Specific 5 (GAS5) Suppresses Esophageal Squamous Cell Carcinoma Cell Proliferation and Migration by Inactivating Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway. Med Sci Monit. 2018;24:7689-7696.
Wang, G., Sun, J., Zhao, H., & Li, H. (2018). Long Non-Coding RNA (lncRNA) Growth Arrest Specific 5 (GAS5) Suppresses Esophageal Squamous Cell Carcinoma Cell Proliferation and Migration by Inactivating Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway. Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, 24, pp. 7689-7696. doi:10.12659/MSM.910867.
Wang G, et al. Long Non-Coding RNA (lncRNA) Growth Arrest Specific 5 (GAS5) Suppresses Esophageal Squamous Cell Carcinoma Cell Proliferation and Migration By Inactivating Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway. Med Sci Monit. 2018 Oct 28;24:7689-7696. PubMed PMID: 30368517.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Long Non-Coding RNA (lncRNA) Growth Arrest Specific 5 (GAS5) Suppresses Esophageal Squamous Cell Carcinoma Cell Proliferation and Migration by Inactivating Phosphatidylinositol 3-kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway. AU - Wang,Guojun, AU - Sun,Junfeng, AU - Zhao,Hongchao, AU - Li,Haohao, Y1 - 2018/10/28/ PY - 2018/10/29/entrez PY - 2018/10/29/pubmed PY - 2019/1/8/medline SP - 7689 EP - 7696 JF - Medical science monitor : international medical journal of experimental and clinical research JO - Med. Sci. Monit. VL - 24 N2 - BACKGROUND lncRNA GAS5 acts as a tumor-suppressor gene in various types of malignancies, but its involvement in esophageal cancer has not been well studied. MATERIAL AND METHODS A total of 112 patients with esophageal cancer and 55 volunteers with normal physiological conditions were included in this study. Tumor tissues and adjacent healthy tissues were collected from esophageal cancer patients and blood was extracted from patients and controls. Expression of GAS5 in those tissues was detected by qRT-PCR. All patients were followed up for 5 years and diagnostic and prognostic values of serum GAS5 for esophageal cancer were investigated by ROC curve analysis and survival curve analysis, respectively. Effects of GAS5 expression on cell proliferation and migration were investigated by CCK-8 assay and Transwell cell migration assay, respectively. Effects of GAS5 overexpression on expression of PI3K/AKT/mTOR-related proteins were explored by Western blot analysis. RESULTS GAS5 expression level was lower in tumor tissues than in adjacent healthy tissues. Serum level of GAS5 was lower in cancer patients than in healthy controls, and serum level of GAS5 was decreased with increase in stage of primary tumor (T stage). GAS5 overexpression inhibited tumor cell proliferation and migration, while treatment with PI3K activator reduced the inhibitory effects. GAS5 overexpression decreased the expression level of PI3K and phosphorylation levels of Akt and mTOR in esophageal cancer cells, while PI3K activator treatment showed no significant effects on GAS5 expression. CONCLUSIONS GAS5 was downregulated in esophageal cancer patients compared to healthy controls, and GAS5 overexpression suppressed proliferation and migration of esophageal cancer cells by inactivating the PI3K/AKT/mTOR pathway. SN - 1643-3750 UR - https://www.unboundmedicine.com/medline/citation/30368517/Long_Non_Coding_RNA__lncRNA__Growth_Arrest_Specific_5__GAS5__Suppresses_Esophageal_Squamous_Cell_Carcinoma_Cell_Proliferation_and_Migration_by_Inactivating_Phosphatidylinositol_3_kinase__PI3K_/AKT/Mammalian_Target_of_Rapamycin__mTOR__Signaling_Pathway_ L2 - https://www.medscimonit.com/download/index/idArt/910867 DB - PRIME DP - Unbound Medicine ER -