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Antitumor effect of temsirolimus against oral squamous cell carcinoma associated with bone destruction
Tatsuo Okui1, Tsuyoshi Shimo, Takuya Fukazawa
1Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama, 700-8525, Japan.
Abstract:
The mammalian target of rapamycin (mTOR) is engaged in the molecular pathogenesis of oral squamous cell carcinoma, which frequently invades the maxilla or the mandible. However, the effects of a mTOR inhibitor on bone destruction associated with oral squamous cell carcinoma are still unclear. In this study, we investigated the antitumor effect of temsirolimus-mediated mTOR inhibition against advanced oral squamous cell carcinoma. Temsirolimus inhibited the proliferation and migration of HSC-2 oral squamous cell carcinoma cells in vitro and suppressed the growth of oral squamous cell carcinoma xenografts in vivo. Significantly, we clearly show that temsirolimus inhibited osteoclast formation both in vitro and in vivo. Reverse transcriptase-PCR analysis showed that temsirolimus decreased the mRNA expression of receptor activator for nuclear factor-κB ligand, known as an osteoclast differentiation factor in bone stromal ST2 cells. Moreover, temsirolimus normalized blood-free calcium concentration in mouse models for humoral hypercalcemia. These findings suggest that mTOR signaling is a potential target of oral squamous cell carcinoma associated with bone destruction, and hence we describe the efficacy of temsirolimus for the treatment of advanced oral squamous carcinoma.
Insights
Temsirolimus, an mTOR inhibitor, combats oral squamous cell carcinoma by reducing tumor growth and inhibiting bone destruction. This drug shows promise in treating advanced oral cancer with bone invasion.
Area of Science:
- Oncology
- Molecular Biology
- Bone Biology
Background:
- Mammalian target of rapamycin (mTOR) signaling is implicated in oral squamous cell carcinoma (OSCC) pathogenesis.
- OSCC frequently invades the maxilla or mandible, leading to bone destruction.
- The impact of mTOR inhibitors on OSCC-associated bone destruction remains unclear.
Purpose of the Study:
- To investigate the antitumor effects of temsirolimus-mediated mTOR inhibition in advanced OSCC.
- To evaluate the impact of temsirolimus on bone destruction associated with OSCC.
Main Methods:
- In vitro studies using HSC-2 OSCC cells to assess proliferation and migration.
- In vivo studies using OSCC xenograft models.
- Assessment of osteoclast formation and receptor activator of nuclear factor-κB ligand (RANKL) mRNA expression.
- Evaluation of serum calcium levels in mouse models of humoral hypercalcemia.
Main Results:
- Temsirolimus inhibited OSCC cell proliferation and migration in vitro.
- Temsirolimus suppressed OSCC xenograft growth in vivo.
- Temsirolimus significantly inhibited osteoclast formation both in vitro and in vivo.
- Temsirolimus reduced RANKL mRNA expression in bone stromal cells.
- Temsirolimus normalized hypercalcemia in mouse models.
Conclusions:
- mTOR signaling is a viable therapeutic target for OSCC with bone destruction.
- Temsirolimus demonstrates efficacy in treating advanced OSCC, including its bone-destructive aspects.
- Targeting mTOR may offer a novel therapeutic strategy for OSCC patients with skeletal involvement.
