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Cholangiocarcinoma cells express somatostatin receptor subtype 2 and respond to octreotide treatment
1Department of General Surgery, People's Hospital, Peking University, XiZhiMenNan Street 11#, Beijing 100044, China.
Background/Purpose:
We investigated the in vitro and in vivo inhibitory effects of a somatostatin analogue (octreotide, OCT) on cholangiocarcinoma cell lines.
Methods:
The reverse transcriptase-polymerase chain reaction (RT-PCR) was employed to detect the gene expression of five somatostatin receptor (SSTR) subtypes in four cholangiocarcinoma cell lines (RBE, NEC, QBC939, and SSP-25). The antiproliferative effects of OCT on these cell lines were determined by means of an MTT assay in vitro, as well as in a nude mouse tumor heterograft model in vivo. Apoptosis and cell cycles in the cholangiocarcinoma cell lines after OCT administration were evaluated by flow cytometry; and the effects of OCT on the expression of cyclin E, cyclin-dependent kinase 2 (CDK2), and p27kipl were evaluated by Western blots.
Results:
Only SSTR2 mRNA was detected in these four cholangiocarcinoma cell lines. OCT significantly inhibited the proliferation of the four cholangiocarcinoma cell lines in vitro ( P < 0.05 vs control), and the weights of the QBC939 xenografts in the OCT-treated group were lower than those in the control group, but there was no significant difference between them. After 48-h exposure to 10(3) ng/ml OCT, flow cytometric analysis demonstrated an increased number of cells in G0/G1 phase associated with a decreased number of cells in G2/M and S phases ( P < 0.01 vs control). Apoptosis was not observed in any samples. The expression of p27kipl was promoted by OCT administration, while that of cyclin E and that of CDK2 were inhibited.
Conclusions:
The results proved that OCT inhibits the proliferation of cholangiocarcinoma cells through G0/G1 cell cycle arrest rather than through the process of apoptosis. These effects are partially mediated by enhancing the expression of p27kipl, and decreasing the amounts of cyclin E-CDK2 complex.
Insights
Octreotide (OCT) inhibits cholangiocarcinoma cell growth by arresting the cell cycle at G0/G1 phase, not by inducing apoptosis. This effect is linked to increased p27kipl and decreased cyclin E-CDK2 complex expression.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Cholangiocarcinoma is a challenging cancer with limited treatment options.
- Somatostatin analogues like octreotide (OCT) show potential in inhibiting cancer cell growth.
Purpose of the Study:
- To investigate the in vitro and in vivo effects of octreotide (OCT) on cholangiocarcinoma cell lines.
- To determine the mechanism of OCT's action on cholangiocarcinoma cell proliferation, cell cycle, and apoptosis.
Main Methods:
- Gene expression of somatostatin receptor (SSTR) subtypes was analyzed using RT-PCR.
- Antiproliferative effects were assessed via MTT assay (in vitro) and xenograft models (in vivo).
- Cell cycle distribution and apoptosis were evaluated by flow cytometry; protein expression by Western blot.
Main Results:
- Only SSTR2 mRNA was detected in cholangiocarcinoma cell lines.
- OCT significantly inhibited cholangiocarcinoma cell proliferation in vitro.
- OCT induced G0/G1 cell cycle arrest, without significant apoptosis, and modulated p27kipl, cyclin E, and CDK2 expression.
Conclusions:
- Octreotide inhibits cholangiocarcinoma cell proliferation primarily through G0/G1 cell cycle arrest.
- The mechanism involves upregulation of p27kipl and downregulation of the cyclin E-CDK2 complex.
- OCT demonstrates potential as a therapeutic agent for cholangiocarcinoma.
