MicroRNA-17-5p Regulation of Apoptosis-Related Protein Expressions in Oral Squam ous Cell Ca rcinoma Cells Is Related to Betel Quid Chewing

Chi-Yeh Lin, Chun-You Chen, Chiu-Ping Chen, Chih-Cheng Chou, Tzu-Hsin Chen, Yi Ju Chen, Hao Wang, Chun-I Li, Chia Yi Tsai, Chia Hui Chen, Szu-Yuan Wu

Research output: Contribution to journalArticle

Abstract

Background and purpose : Betel nut chewing is associated with oral cavity cancer in Taiwan. Radiotherapy is one of the therapeutic approaches. Our previous study demonstrated that microRNA (miR)-17-5p (one of the miR-17-92 polycistronic miRNAs) was enhanced in the irradiated OC3 cancer cell line (which was established from oral squamous cell carcinoma in a long-term betel nut chewer who did not smoke), and miR-17-5p was also found to inhibit downstream protein p21 expression and induce radiosensitivity. In this study, we used a human apoptosis protein array to clarify which apoptosis-related proteins are modulated by miR-17-5p. Materials and Methods : Total cell lysates from OC3 cells with control small interfering (si)RNA or miR-17-5p were used to analyze apoptosis-related proteins. A specific miR- 17-5p effector apoptosis-related protein was confirmed by Western blotting. To confirm the role of p53 in irradiated OC-3 cells, OC3 cells without or with a p53-overexpressing clone were irradiated and examined by propidium iodide staining and flow cytometry. Results : Using a human apoptosis protein array analysis (R&D Systems; catalog # ARY009), we simultaneously detected the relative expressions of 35 apoptosis-related proteins in OC3 cells that were treated with an miR-17-5p antisense oligonucleotide (AS-ODN) or a control ODN. Several proteins, including p21, p53, TNF RI, FADD, cIAP-1, HIF-1α, and TRAIL R1, were found to be up- or downregulated by miR-17-5p in OC3 cells; their expression patterns were also confirmed by Western blotting. We further clarified the role of p53 in irradiated OC3 cells, using a p53 overexpression strategy, and results revealed that enhancement of p53 expression significantly enhanced radiation-induced G2/M arrest of OC3 cells. Conclusions : miR-17-5p regulated the apoptosis-related proteins of p21, p53, TNF RI, FADD, cIAP-1, HIF-1α, and TRAIL R1 in OC3 cells; interestingly, its effect on p53 protein expression contributed to modulating the cell cycle arrest of OC3 cells.
Original languageEnglish
Pages (from-to)255-266
Number of pages12
Journal放射治療與腫瘤學
Volume22
Issue number4
DOIs
Publication statusPublished - 2015

Fingerprint

Mastication
MicroRNAs
Apoptosis
Proteins
Areca
Protein Array Analysis
Western Blotting
Propidium
Antisense Oligonucleotides
Mouth Neoplasms
Radiation Tolerance
Cell Cycle Checkpoints
Taiwan
Smoke
Small Interfering RNA
Mouth
Squamous Cell Carcinoma
Flow Cytometry
Radiotherapy
Down-Regulation

Keywords

  • 微核醣核酸17-5p
  • 放射線
  • OC3細胞
  • p53蛋白
  • MicroRNA (miR)-17-5p
  • Radiation
  • Oral carcinoma 3 (OC3) cells
  • Tumor protein p53

Cite this

MicroRNA-17-5p Regulation of Apoptosis-Related Protein Expressions in Oral Squam ous Cell Ca rcinoma Cells Is Related to Betel Quid Chewing. / Lin, Chi-Yeh; Chen, Chun-You; Chen, Chiu-Ping; Chou, Chih-Cheng; Chen, Tzu-Hsin; Chen, Yi Ju; Wang, Hao; Li, Chun-I; Tsai, Chia Yi; Chen, Chia Hui; Wu, Szu-Yuan.

In: 放射治療與腫瘤學, Vol. 22, No. 4, 2015, p. 255-266.

Research output: Contribution to journalArticle

Lin, C-Y, Chen, C-Y, Chen, C-P, Chou, C-C, Chen, T-H, Chen, YJ, Wang, H, Li, C-I, Tsai, CY, Chen, CH & Wu, S-Y 2015, 'MicroRNA-17-5p Regulation of Apoptosis-Related Protein Expressions in Oral Squam ous Cell Ca rcinoma Cells Is Related to Betel Quid Chewing', 放射治療與腫瘤學, vol. 22, no. 4, pp. 255-266. https://doi.org/10.6316/TRO/201522
Lin, Chi-Yeh ; Chen, Chun-You ; Chen, Chiu-Ping ; Chou, Chih-Cheng ; Chen, Tzu-Hsin ; Chen, Yi Ju ; Wang, Hao ; Li, Chun-I ; Tsai, Chia Yi ; Chen, Chia Hui ; Wu, Szu-Yuan. / MicroRNA-17-5p Regulation of Apoptosis-Related Protein Expressions in Oral Squam ous Cell Ca rcinoma Cells Is Related to Betel Quid Chewing. In: 放射治療與腫瘤學. 2015 ; Vol. 22, No. 4. pp. 255-266.
@article{e509916e7b2b481e8a5cf2cf3f31c1c1,
title = "MicroRNA-17-5p Regulation of Apoptosis-Related Protein Expressions in Oral Squam ous Cell Ca rcinoma Cells Is Related to Betel Quid Chewing",
abstract = "Background and purpose : Betel nut chewing is associated with oral cavity cancer in Taiwan. Radiotherapy is one of the therapeutic approaches. Our previous study demonstrated that microRNA (miR)-17-5p (one of the miR-17-92 polycistronic miRNAs) was enhanced in the irradiated OC3 cancer cell line (which was established from oral squamous cell carcinoma in a long-term betel nut chewer who did not smoke), and miR-17-5p was also found to inhibit downstream protein p21 expression and induce radiosensitivity. In this study, we used a human apoptosis protein array to clarify which apoptosis-related proteins are modulated by miR-17-5p. Materials and Methods : Total cell lysates from OC3 cells with control small interfering (si)RNA or miR-17-5p were used to analyze apoptosis-related proteins. A specific miR- 17-5p effector apoptosis-related protein was confirmed by Western blotting. To confirm the role of p53 in irradiated OC-3 cells, OC3 cells without or with a p53-overexpressing clone were irradiated and examined by propidium iodide staining and flow cytometry. Results : Using a human apoptosis protein array analysis (R&D Systems; catalog # ARY009), we simultaneously detected the relative expressions of 35 apoptosis-related proteins in OC3 cells that were treated with an miR-17-5p antisense oligonucleotide (AS-ODN) or a control ODN. Several proteins, including p21, p53, TNF RI, FADD, cIAP-1, HIF-1α, and TRAIL R1, were found to be up- or downregulated by miR-17-5p in OC3 cells; their expression patterns were also confirmed by Western blotting. We further clarified the role of p53 in irradiated OC3 cells, using a p53 overexpression strategy, and results revealed that enhancement of p53 expression significantly enhanced radiation-induced G2/M arrest of OC3 cells. Conclusions : miR-17-5p regulated the apoptosis-related proteins of p21, p53, TNF RI, FADD, cIAP-1, HIF-1α, and TRAIL R1 in OC3 cells; interestingly, its effect on p53 protein expression contributed to modulating the cell cycle arrest of OC3 cells.",
keywords = "微核醣核酸17-5p, 放射線, OC3細胞, p53蛋白, MicroRNA (miR)-17-5p, Radiation, Oral carcinoma 3 (OC3) cells, Tumor protein p53",
author = "Chi-Yeh Lin and Chun-You Chen and Chiu-Ping Chen and Chih-Cheng Chou and Tzu-Hsin Chen and Chen, {Yi Ju} and Hao Wang and Chun-I Li and Tsai, {Chia Yi} and Chen, {Chia Hui} and Szu-Yuan Wu",
year = "2015",
doi = "10.6316/TRO/201522",
language = "English",
volume = "22",
pages = "255--266",
journal = "放射治療與腫瘤學",
issn = "1023-988x",
publisher = "台灣放射腫瘤學會",
number = "4",

}

TY - JOUR

T1 - MicroRNA-17-5p Regulation of Apoptosis-Related Protein Expressions in Oral Squam ous Cell Ca rcinoma Cells Is Related to Betel Quid Chewing

AU - Lin, Chi-Yeh

AU - Chen, Chun-You

AU - Chen, Chiu-Ping

AU - Chou, Chih-Cheng

AU - Chen, Tzu-Hsin

AU - Chen, Yi Ju

AU - Wang, Hao

AU - Li, Chun-I

AU - Tsai, Chia Yi

AU - Chen, Chia Hui

AU - Wu, Szu-Yuan

PY - 2015

Y1 - 2015

N2 - Background and purpose : Betel nut chewing is associated with oral cavity cancer in Taiwan. Radiotherapy is one of the therapeutic approaches. Our previous study demonstrated that microRNA (miR)-17-5p (one of the miR-17-92 polycistronic miRNAs) was enhanced in the irradiated OC3 cancer cell line (which was established from oral squamous cell carcinoma in a long-term betel nut chewer who did not smoke), and miR-17-5p was also found to inhibit downstream protein p21 expression and induce radiosensitivity. In this study, we used a human apoptosis protein array to clarify which apoptosis-related proteins are modulated by miR-17-5p. Materials and Methods : Total cell lysates from OC3 cells with control small interfering (si)RNA or miR-17-5p were used to analyze apoptosis-related proteins. A specific miR- 17-5p effector apoptosis-related protein was confirmed by Western blotting. To confirm the role of p53 in irradiated OC-3 cells, OC3 cells without or with a p53-overexpressing clone were irradiated and examined by propidium iodide staining and flow cytometry. Results : Using a human apoptosis protein array analysis (R&D Systems; catalog # ARY009), we simultaneously detected the relative expressions of 35 apoptosis-related proteins in OC3 cells that were treated with an miR-17-5p antisense oligonucleotide (AS-ODN) or a control ODN. Several proteins, including p21, p53, TNF RI, FADD, cIAP-1, HIF-1α, and TRAIL R1, were found to be up- or downregulated by miR-17-5p in OC3 cells; their expression patterns were also confirmed by Western blotting. We further clarified the role of p53 in irradiated OC3 cells, using a p53 overexpression strategy, and results revealed that enhancement of p53 expression significantly enhanced radiation-induced G2/M arrest of OC3 cells. Conclusions : miR-17-5p regulated the apoptosis-related proteins of p21, p53, TNF RI, FADD, cIAP-1, HIF-1α, and TRAIL R1 in OC3 cells; interestingly, its effect on p53 protein expression contributed to modulating the cell cycle arrest of OC3 cells.

AB - Background and purpose : Betel nut chewing is associated with oral cavity cancer in Taiwan. Radiotherapy is one of the therapeutic approaches. Our previous study demonstrated that microRNA (miR)-17-5p (one of the miR-17-92 polycistronic miRNAs) was enhanced in the irradiated OC3 cancer cell line (which was established from oral squamous cell carcinoma in a long-term betel nut chewer who did not smoke), and miR-17-5p was also found to inhibit downstream protein p21 expression and induce radiosensitivity. In this study, we used a human apoptosis protein array to clarify which apoptosis-related proteins are modulated by miR-17-5p. Materials and Methods : Total cell lysates from OC3 cells with control small interfering (si)RNA or miR-17-5p were used to analyze apoptosis-related proteins. A specific miR- 17-5p effector apoptosis-related protein was confirmed by Western blotting. To confirm the role of p53 in irradiated OC-3 cells, OC3 cells without or with a p53-overexpressing clone were irradiated and examined by propidium iodide staining and flow cytometry. Results : Using a human apoptosis protein array analysis (R&D Systems; catalog # ARY009), we simultaneously detected the relative expressions of 35 apoptosis-related proteins in OC3 cells that were treated with an miR-17-5p antisense oligonucleotide (AS-ODN) or a control ODN. Several proteins, including p21, p53, TNF RI, FADD, cIAP-1, HIF-1α, and TRAIL R1, were found to be up- or downregulated by miR-17-5p in OC3 cells; their expression patterns were also confirmed by Western blotting. We further clarified the role of p53 in irradiated OC3 cells, using a p53 overexpression strategy, and results revealed that enhancement of p53 expression significantly enhanced radiation-induced G2/M arrest of OC3 cells. Conclusions : miR-17-5p regulated the apoptosis-related proteins of p21, p53, TNF RI, FADD, cIAP-1, HIF-1α, and TRAIL R1 in OC3 cells; interestingly, its effect on p53 protein expression contributed to modulating the cell cycle arrest of OC3 cells.

KW - 微核醣核酸17-5p

KW - 放射線

KW - OC3細胞

KW - p53蛋白

KW - MicroRNA (miR)-17-5p

KW - Radiation

KW - Oral carcinoma 3 (OC3) cells

KW - Tumor protein p53

UR - http://www.airitilibrary.com/Publication/alDetailedMesh?DocID=1023988x-201512-201601220002-201601220002-255-266

U2 - 10.6316/TRO/201522

DO - 10.6316/TRO/201522

M3 - Article

VL - 22

SP - 255

EP - 266

JO - 放射治療與腫瘤學

JF - 放射治療與腫瘤學

SN - 1023-988x

IS - 4

ER -