Chitosan exerts anticancer activity through induction of apoptosis and cell cycle arrest in oral cancer cells

Yuniardini Septorini Wimardhani, Dewi Fatma Suniarti Sastradipura, Hans J. Freisleben, Septelia Inawati Wanandi, Nuryati Chairani Siregar, Masa Aki Ikeda

Research output: Contribution to journalArticlepeer-review

59 Citations (Scopus)


Chitosan, a multipurpose biomaterial, has been shown to exert effects against several types of cancer including oral cancer. However, the mechanisms underlying the anticancer activities of chitosan on oral squamous cell carcinoma (SCC) cells remain largely unknown. The present study aimed to compare the effects of low-molecular-weight chitosan (LMWC) and cisplatin on oral SCC Ca9-22 and noncancer keratinocyte HaCaT cell lines. Cell viability and cell cycle profiles were measured by MTT assay and laser scanning cytometry, respectively. Apoptosis was examined by TUNEL assay and electron microscopy, followed by analysis of caspase activity. LMWC exhibited cytotoxic effects on Ca9-22, but not HaCaT cells, whereas cisplatin induced apoptosis in both types of cells. Exposure of Ca9-22 cells to LMWC led to G1/S cell cycle arrest and an increase of TUNELpositive cells accompanied by an early apoptotic cell morphology and subtle increases of caspase activity. Short-term LMWC exposure was less cytotoxic to HaCaT cells than to Ca9-22 cells, and anticancer activity was exerted through induction of apoptosis and cell cycle arrest, suggesting that LMWC could be a promising natural anticancer agent with fewer side effects on normal cells.

Original languageEnglish
Pages (from-to)119-126
Number of pages8
JournalJournal of Oral Science
Issue number2
Publication statusPublished - 13 Jun 2014


  • Apoptosis
  • Cell cycle
  • Chitosan
  • Electron microscopy
  • Oral cancer
  • Proliferation


Dive into the research topics of 'Chitosan exerts anticancer activity through induction of apoptosis and cell cycle arrest in oral cancer cells'. Together they form a unique fingerprint.

Cite this