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Published on: September 30, 2016
Effects of octreotide and insulin on colon cancer cellular proliferation and correlation with hTERT activity
Georgios D Ayiomamitis1, George Notas2, Apostolos Zaravinos3
1Laboratory of Gastroenterology, School of Medicine, University of Crete, Heraklion, Greece ; 2nd Department of Surgery, Tzaneion General Hospital, Piraeus, Greece.
Abstract:
Peptide hormone somatostatin and its receptors have a wide range of physiological functions and play a role in the treatment of numerous human diseases, including colorectal cancer. Octreotide, a synthetic somatostatin-analog peptide, inhibits growth of colonic cancer cells primarily by binding to G-protein coupled receptors and elicits cellular responses through second-messenger systems. Insulin also initiates mitogenic signals in certain cell types. The objective of the present study was to explore the effects of octreotide with or without insulin treatment, on Caco-2 and HT-29 human colon-cancer cell proliferation and to correlate their effects with the activation of telomerase reverse transcriptase (hTERT). The involvement of protein tyrosine phosphatases in the regulation of the anti-proliferative effect of octreotide was also evaluated. Sodium orthovanadate was used to reverse the anti- proliferative effect of octreotide. Telomerase activity was determined for each time point under octreotide and/or insulin treatment. Elevated expression of sst1, sst2 and sst5 was confirmed in both cell lines by RT-PCR. Immunocytochemistry detected sst1, sst2A, sst2B, sst3, sst4 and sst5 protein expression in the membranes of both cell lines. Octreotide inhibited the proliferation of Caco-2 and HT-29 cells in a time and dose-dependent manner. Insulin exerted proliferative effects in Caco-2 cells and octreotide reversed its effect in both cell lines. Sodium orthovanadate suppressed the anti-proliferative effect of octreotide both in Caco-2 and HT-29 cells. Telomerase activity was significantly reduced when Caco-2 cells were exposed to octreotide, under serum-free cultured medium. On the other hand, telomerase attenuation after octreotide treatment could not counteract the actions of insulin on both cells. Our data indicate that the use of octreotide could provide a possible therapeutic approach to the management of certain patients who suffer from colon cancer.
Insights
Octreotide, a somatostatin analog, inhibits colon cancer cell growth by affecting telomerase activity. While insulin promotes proliferation, octreotide reverses this effect, suggesting therapeutic potential for colorectal cancer.
Area of Science:
- Endocrinology
- Oncology
- Molecular Biology
Background:
- Somatostatin analogs like octreotide are used in cancer therapy.
- Insulin can promote cancer cell proliferation.
- Telomerase is a key enzyme in cancer cell immortalization.
Purpose of the Study:
- To investigate octreotide's effect on colon cancer cell proliferation, with or without insulin.
- To correlate these effects with telomerase reverse transcriptase (hTERT) activation.
- To evaluate the role of protein tyrosine phosphatases in octreotide's anti-proliferative action.
Main Methods:
- Utilized Caco-2 and HT-29 human colon cancer cell lines.
- Administered octreotide and/or insulin, with sodium orthovanadate to assess protein tyrosine phosphatase involvement.
- Measured cell proliferation, telomerase activity, and receptor expression (sst1, sst2, sst5) via RT-PCR and immunocytochemistry.
Main Results:
- Octreotide inhibited colon cancer cell proliferation dose- and time-dependently.
- Insulin stimulated proliferation in Caco-2 cells, an effect reversed by octreotide.
- Octreotide reduced telomerase activity, but this effect did not fully counteract insulin's proliferative actions.
Conclusions:
- Octreotide demonstrates anti-proliferative effects on colon cancer cells, partly via telomerase modulation.
- Octreotide can counteract insulin-induced proliferation in these cells.
- Octreotide presents a potential therapeutic strategy for managing colorectal cancer.
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