Enhanced cisplatin resistance in oral-cancer stem-like cells is correlated with upregulation of excision-repair cross-complementation group 1

Lo-Lin Tsai, Cheng Chia Yu, Jeng Fan Lo, Wen Wei Sung, Huei Lee, Shiow Ling Chen, Ming Yung Chou

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background/purpose: Oral squamous cell carcinoma (OSCC) is a prevalent cancer worldwide. Recent data suggest that a subpopulation of cancer cells, termed cancer stem cells (CSCs), is capable of initiating, maintaining, and expanding the growth of tumors. Importantly, CSCs confer chemo- and radioresistance. Cisplatin is the most widely used chemotherapeutic agent, and chemoresistance to cisplatin is one of the major causes of tumor recurrence and metastasis with OSCC. However, the role of oral-cancer stem-like cells (OC-SLCs) in the chemoresistance of OSCC has not determined. The aim of this study was to investigate a key player of chemoresistance in OC-SLCs. Materials and methods: OC-SLCs were isolated through sphere formation by cultivating the OC2 cell line in defined serum-free medium. Differential expression profiles of cell-surface stemness markers between enriched OC-SLCs and parental OSCC cells were elucidated by flow cytometry. Expression of excision repair cross- complementation group 1 (ERCC1) by OC-SLCs was examined by an RT-PCR and Western blotting. Results: Initially, significant sphere formation (OC-SLCs) was observed in OC2 cells. Enriched OC-SLCs highly expressed stem-cell surface markers (CD117 and CD133) and the ABC transporter gene (ABCG2). Enhanced chemoresistance to cisplatin was also noted in OC-SLCs. Further, the chemoresistance of OC-SLCs to cisplatin was possibly correlated with ERCC1 upregulation in OC-SLCs. Conclusions: In summary, these results suggest that OC-SLCs may play a vital role in tumor recurrence due to resistance to cisplatin. Additionally, ERCC1 upregulation might be involved in platinum resistance in oral CSCs.

Original languageEnglish
Pages (from-to)111-117
Number of pages7
JournalJournal of Dental Sciences
Volume7
Issue number2
DOIs
Publication statusPublished - Jun 2012
Externally publishedYes

Fingerprint

Neoplastic Stem Cells
Mouth Neoplasms
DNA Repair
Cisplatin
Up-Regulation
Squamous Cell Carcinoma
Neoplasms
Recurrence
ATP-Binding Cassette Transporters
Serum-Free Culture Media
Platinum
Flow Cytometry

Keywords

  • cancer stem cells
  • chemoresistance
  • ERCC1
  • oral squamous cell carcinoma

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Enhanced cisplatin resistance in oral-cancer stem-like cells is correlated with upregulation of excision-repair cross-complementation group 1. / Tsai, Lo-Lin; Yu, Cheng Chia; Lo, Jeng Fan; Sung, Wen Wei; Lee, Huei; Chen, Shiow Ling; Chou, Ming Yung.

In: Journal of Dental Sciences, Vol. 7, No. 2, 06.2012, p. 111-117.

Research output: Contribution to journalArticle

Tsai, Lo-Lin ; Yu, Cheng Chia ; Lo, Jeng Fan ; Sung, Wen Wei ; Lee, Huei ; Chen, Shiow Ling ; Chou, Ming Yung. / Enhanced cisplatin resistance in oral-cancer stem-like cells is correlated with upregulation of excision-repair cross-complementation group 1. In: Journal of Dental Sciences. 2012 ; Vol. 7, No. 2. pp. 111-117.
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abstract = "Background/purpose: Oral squamous cell carcinoma (OSCC) is a prevalent cancer worldwide. Recent data suggest that a subpopulation of cancer cells, termed cancer stem cells (CSCs), is capable of initiating, maintaining, and expanding the growth of tumors. Importantly, CSCs confer chemo- and radioresistance. Cisplatin is the most widely used chemotherapeutic agent, and chemoresistance to cisplatin is one of the major causes of tumor recurrence and metastasis with OSCC. However, the role of oral-cancer stem-like cells (OC-SLCs) in the chemoresistance of OSCC has not determined. The aim of this study was to investigate a key player of chemoresistance in OC-SLCs. Materials and methods: OC-SLCs were isolated through sphere formation by cultivating the OC2 cell line in defined serum-free medium. Differential expression profiles of cell-surface stemness markers between enriched OC-SLCs and parental OSCC cells were elucidated by flow cytometry. Expression of excision repair cross- complementation group 1 (ERCC1) by OC-SLCs was examined by an RT-PCR and Western blotting. Results: Initially, significant sphere formation (OC-SLCs) was observed in OC2 cells. Enriched OC-SLCs highly expressed stem-cell surface markers (CD117 and CD133) and the ABC transporter gene (ABCG2). Enhanced chemoresistance to cisplatin was also noted in OC-SLCs. Further, the chemoresistance of OC-SLCs to cisplatin was possibly correlated with ERCC1 upregulation in OC-SLCs. Conclusions: In summary, these results suggest that OC-SLCs may play a vital role in tumor recurrence due to resistance to cisplatin. Additionally, ERCC1 upregulation might be involved in platinum resistance in oral CSCs.",
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AU - Tsai, Lo-Lin

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AU - Sung, Wen Wei

AU - Lee, Huei

AU - Chen, Shiow Ling

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AB - Background/purpose: Oral squamous cell carcinoma (OSCC) is a prevalent cancer worldwide. Recent data suggest that a subpopulation of cancer cells, termed cancer stem cells (CSCs), is capable of initiating, maintaining, and expanding the growth of tumors. Importantly, CSCs confer chemo- and radioresistance. Cisplatin is the most widely used chemotherapeutic agent, and chemoresistance to cisplatin is one of the major causes of tumor recurrence and metastasis with OSCC. However, the role of oral-cancer stem-like cells (OC-SLCs) in the chemoresistance of OSCC has not determined. The aim of this study was to investigate a key player of chemoresistance in OC-SLCs. Materials and methods: OC-SLCs were isolated through sphere formation by cultivating the OC2 cell line in defined serum-free medium. Differential expression profiles of cell-surface stemness markers between enriched OC-SLCs and parental OSCC cells were elucidated by flow cytometry. Expression of excision repair cross- complementation group 1 (ERCC1) by OC-SLCs was examined by an RT-PCR and Western blotting. Results: Initially, significant sphere formation (OC-SLCs) was observed in OC2 cells. Enriched OC-SLCs highly expressed stem-cell surface markers (CD117 and CD133) and the ABC transporter gene (ABCG2). Enhanced chemoresistance to cisplatin was also noted in OC-SLCs. Further, the chemoresistance of OC-SLCs to cisplatin was possibly correlated with ERCC1 upregulation in OC-SLCs. Conclusions: In summary, these results suggest that OC-SLCs may play a vital role in tumor recurrence due to resistance to cisplatin. Additionally, ERCC1 upregulation might be involved in platinum resistance in oral CSCs.

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