Sam68 reduces cisplatin-induced apoptosis in tongue carcinoma

Shuwei Chen, Huan Li, Shimin Zhuang, Ji Zhang, Fan Gao, Xidi Wang, Wenkuan Chen, Ming Song

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Background: Resistance to anticancer agents is a major obstacle for successful chemotherapy in tongue squamous cancer. Sam68 is an oncogenic-related protein in oral tongue squamous cell carcinoma functions as a signaling molecule mediating apoptosis, whose over-expression is associated with the clinicopathologic characteristics and prognosis of patients. The present study was to examine the effect of Sam68 on chemotherapeutics-induced apoptosis in oral tongue squamous cell carcinoma, and its clinical significance in oral tongue squamous cell carcinoma progression. Methods: The effect of Sam68 on apoptosis induced by cisplatin was examined both in vitro and in vivo, using Annexin V staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assays. Real-time PCR and Western blotting analysis were used to detect mRNA and protein expression levels. Results: Upregulation of Sam68 significantly inhibited cisplatin-induced apoptosis in oral tongue squamous cell carcinoma cells, associated with induction of anti-apoptotic proteins caspase-9, caspase-3, and PARP. In contrast, Silencing Sam68 expression significantly enhanced the sensitivity of oral tongue squamous cell carcinoma cells to apoptosis induced by cisplatin both in vitro and in vivo. Conclusions: The current study suggests that Sam68 could enhance the anti-apoptosis activity of oral tongue squamous cell carcinoma cells. Sam68 is a potential pharmacologic target for the treatment of oral tongue squamous cell carcinoma and inhibition of Sam68 expression might represent a novel strategy to sensitize oral tongue squamous cell carcinoma to chemotherapy.

Original languageEnglish (US)
Article number123
JournalJournal of Experimental and Clinical Cancer Research
Volume35
Issue number1
DOIs
StatePublished - Jul 29 2016

Fingerprint

Tongue
Cisplatin
Squamous Cell Carcinoma
Apoptosis
Carcinoma
Tongue Neoplasms
Drug Therapy
Apoptosis Regulatory Proteins
DNA Nucleotidylexotransferase
Caspase 9
Annexin A5
Caspase 3
Antineoplastic Agents
Real-Time Polymerase Chain Reaction
Proteins
Up-Regulation
Western Blotting
Staining and Labeling
Messenger RNA

Keywords

  • Anti-apoptosis
  • Chemotherapy
  • Sam68
  • Tongue squamous cell carcinoma

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Sam68 reduces cisplatin-induced apoptosis in tongue carcinoma. / Chen, Shuwei; Li, Huan; Zhuang, Shimin; Zhang, Ji; Gao, Fan; Wang, Xidi; Chen, Wenkuan; Song, Ming.

In: Journal of Experimental and Clinical Cancer Research, Vol. 35, No. 1, 123, 29.07.2016.

Research output: Contribution to journalArticle

Chen, Shuwei ; Li, Huan ; Zhuang, Shimin ; Zhang, Ji ; Gao, Fan ; Wang, Xidi ; Chen, Wenkuan ; Song, Ming. / Sam68 reduces cisplatin-induced apoptosis in tongue carcinoma. In: Journal of Experimental and Clinical Cancer Research. 2016 ; Vol. 35, No. 1.
@article{df97b73982134a2db48f05bf976eab36,
title = "Sam68 reduces cisplatin-induced apoptosis in tongue carcinoma",
abstract = "Background: Resistance to anticancer agents is a major obstacle for successful chemotherapy in tongue squamous cancer. Sam68 is an oncogenic-related protein in oral tongue squamous cell carcinoma functions as a signaling molecule mediating apoptosis, whose over-expression is associated with the clinicopathologic characteristics and prognosis of patients. The present study was to examine the effect of Sam68 on chemotherapeutics-induced apoptosis in oral tongue squamous cell carcinoma, and its clinical significance in oral tongue squamous cell carcinoma progression. Methods: The effect of Sam68 on apoptosis induced by cisplatin was examined both in vitro and in vivo, using Annexin V staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assays. Real-time PCR and Western blotting analysis were used to detect mRNA and protein expression levels. Results: Upregulation of Sam68 significantly inhibited cisplatin-induced apoptosis in oral tongue squamous cell carcinoma cells, associated with induction of anti-apoptotic proteins caspase-9, caspase-3, and PARP. In contrast, Silencing Sam68 expression significantly enhanced the sensitivity of oral tongue squamous cell carcinoma cells to apoptosis induced by cisplatin both in vitro and in vivo. Conclusions: The current study suggests that Sam68 could enhance the anti-apoptosis activity of oral tongue squamous cell carcinoma cells. Sam68 is a potential pharmacologic target for the treatment of oral tongue squamous cell carcinoma and inhibition of Sam68 expression might represent a novel strategy to sensitize oral tongue squamous cell carcinoma to chemotherapy.",
keywords = "Anti-apoptosis, Chemotherapy, Sam68, Tongue squamous cell carcinoma",
author = "Shuwei Chen and Huan Li and Shimin Zhuang and Ji Zhang and Fan Gao and Xidi Wang and Wenkuan Chen and Ming Song",
year = "2016",
month = "7",
day = "29",
doi = "10.1186/s13046-016-0390-3",
language = "English (US)",
volume = "35",
journal = "Journal of Experimental and Clinical Cancer Research",
issn = "0392-9078",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - Sam68 reduces cisplatin-induced apoptosis in tongue carcinoma

AU - Chen, Shuwei

AU - Li, Huan

AU - Zhuang, Shimin

AU - Zhang, Ji

AU - Gao, Fan

AU - Wang, Xidi

AU - Chen, Wenkuan

AU - Song, Ming

PY - 2016/7/29

Y1 - 2016/7/29

N2 - Background: Resistance to anticancer agents is a major obstacle for successful chemotherapy in tongue squamous cancer. Sam68 is an oncogenic-related protein in oral tongue squamous cell carcinoma functions as a signaling molecule mediating apoptosis, whose over-expression is associated with the clinicopathologic characteristics and prognosis of patients. The present study was to examine the effect of Sam68 on chemotherapeutics-induced apoptosis in oral tongue squamous cell carcinoma, and its clinical significance in oral tongue squamous cell carcinoma progression. Methods: The effect of Sam68 on apoptosis induced by cisplatin was examined both in vitro and in vivo, using Annexin V staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assays. Real-time PCR and Western blotting analysis were used to detect mRNA and protein expression levels. Results: Upregulation of Sam68 significantly inhibited cisplatin-induced apoptosis in oral tongue squamous cell carcinoma cells, associated with induction of anti-apoptotic proteins caspase-9, caspase-3, and PARP. In contrast, Silencing Sam68 expression significantly enhanced the sensitivity of oral tongue squamous cell carcinoma cells to apoptosis induced by cisplatin both in vitro and in vivo. Conclusions: The current study suggests that Sam68 could enhance the anti-apoptosis activity of oral tongue squamous cell carcinoma cells. Sam68 is a potential pharmacologic target for the treatment of oral tongue squamous cell carcinoma and inhibition of Sam68 expression might represent a novel strategy to sensitize oral tongue squamous cell carcinoma to chemotherapy.

AB - Background: Resistance to anticancer agents is a major obstacle for successful chemotherapy in tongue squamous cancer. Sam68 is an oncogenic-related protein in oral tongue squamous cell carcinoma functions as a signaling molecule mediating apoptosis, whose over-expression is associated with the clinicopathologic characteristics and prognosis of patients. The present study was to examine the effect of Sam68 on chemotherapeutics-induced apoptosis in oral tongue squamous cell carcinoma, and its clinical significance in oral tongue squamous cell carcinoma progression. Methods: The effect of Sam68 on apoptosis induced by cisplatin was examined both in vitro and in vivo, using Annexin V staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assays. Real-time PCR and Western blotting analysis were used to detect mRNA and protein expression levels. Results: Upregulation of Sam68 significantly inhibited cisplatin-induced apoptosis in oral tongue squamous cell carcinoma cells, associated with induction of anti-apoptotic proteins caspase-9, caspase-3, and PARP. In contrast, Silencing Sam68 expression significantly enhanced the sensitivity of oral tongue squamous cell carcinoma cells to apoptosis induced by cisplatin both in vitro and in vivo. Conclusions: The current study suggests that Sam68 could enhance the anti-apoptosis activity of oral tongue squamous cell carcinoma cells. Sam68 is a potential pharmacologic target for the treatment of oral tongue squamous cell carcinoma and inhibition of Sam68 expression might represent a novel strategy to sensitize oral tongue squamous cell carcinoma to chemotherapy.

KW - Anti-apoptosis

KW - Chemotherapy

KW - Sam68

KW - Tongue squamous cell carcinoma

UR - http://www.scopus.com/inward/record.url?scp=84980416177&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84980416177&partnerID=8YFLogxK

U2 - 10.1186/s13046-016-0390-3

DO - 10.1186/s13046-016-0390-3

M3 - Article

C2 - 27473117

AN - SCOPUS:84980416177

VL - 35

JO - Journal of Experimental and Clinical Cancer Research

JF - Journal of Experimental and Clinical Cancer Research

SN - 0392-9078

IS - 1

M1 - 123

ER -