STAT3-PTTG11 abrogation inhibits proliferation and induces apoptosis in malignant glioma cells
Lishan Cui1,2, Lanxi Xu3, Guanling Wang3
1Department of Neurosurgery, Xiang'an Branch, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361005, P.R. China.
Abstract:
Pituitary tumor transforming gene 1 (PTTG11) is abundantly expressed in glioma. Our previous study demonstrated that the downregulation of PTTG11 gene expression significantly inhibited the proliferation, migration and invasion ability, and increased the apoptosis of SHG44 glioma cells. However, the molecular mechanisms that regulate PTTG11 and its actions remain elusive. In the present study, CCK-8 and flow cytometry assays were used to assess the proliferation/viability and apoptosis, respectively, of the human glioma U251 cell line. STAT3-PTTG1 signals were further evaluated by western blotting. The findings of the present study revealed that STAT3 induced PTTG11 expression, which subsequently induced downstream c-Myc and Bcl-2 expression while inhibiting Bax expression, thereby promoting cell viability and inhibiting apoptosis. PTTG11 suppression via siRNA inhibited the viability and increased the apoptosis of glioma cells induced by the STAT3 activator S3I-201. c-Myc and Bcl-2 expression was suppressed by PTTG11 inhibition. The findings of the present study suggest that the STAT3-PTTG11 signaling pathway may play an important role in glioma progression by regulating cell proliferation and apoptosis.
Insights
The STAT3-PTTG11 pathway promotes glioma cell viability and inhibits apoptosis. Inhibiting PTTG11 (Pituitary tumor transforming gene 1) blocks these effects, suggesting a therapeutic target for glioma.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Pituitary tumor transforming gene 1 (PTTG11) is highly expressed in glioma.
- PTTG11 downregulation inhibits glioma cell proliferation and invasion while increasing apoptosis.
- The regulatory mechanisms and downstream effects of PTTG11 in glioma remain unclear.
Purpose of the Study:
- To investigate the role of STAT3 in regulating PTTG11 expression.
- To elucidate the downstream signaling molecules affected by PTTG11.
- To evaluate the therapeutic potential of targeting the STAT3-PTTG11 pathway in glioma.
Main Methods:
- Cell viability was assessed using CCK-8 assays.
- Apoptosis was analyzed via flow cytometry.
- Protein expression levels were determined by western blotting.
Main Results:
- STAT3 activation led to increased PTTG11 expression in glioma cells.
- PTTG11 induced c-Myc and Bcl-2 expression while suppressing Bax, promoting cell viability and inhibiting apoptosis.
- PTTG11 inhibition via siRNA reversed the effects of STAT3 activation, reducing cell viability and increasing apoptosis.
Conclusions:
- The STAT3-PTTG11 signaling pathway is a key regulator of glioma cell proliferation and apoptosis.
- Targeting PTTG11 may represent a novel therapeutic strategy for glioma treatment.
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