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Nicotinic acid impairs assembly of leading edge in glioma cells

Xiangcai Yang¹, Shuting Mei², Hua Niu¹

¹Department of Clinical Laboratory, The Affiliated Hospital of KMUST, Medical Faculty, Kunming University of Science and Technology, Kunming, Yunnan 650032, P.R. China.

Oncology Reports

|June 29, 2017

Abstract:

Malignant glioma is a clinically formidable disease. It commonly leads to death within 5 years after diagnosis. Physicians are often baffled since the inevitable diffuse invasion deteriorates clinical outcomes rapidly. Therefore, cancerous infiltration presents a foremost challenge to all therapeutic strategies on glioblastoma multiforme (GBM). Previously, we demonstrated that nicotinic acid (NA) possesses a brand new function by targeting F-actin stress fibers. By treating HEK293 or NIH3T3 cells with a certain concentration of NA, the F-actin stress fiber was significantly disassembled. This notable finding inspired us to explore NA further in cancer cell lines, such as GBM cells, since F-actin stress fibers are the critical foundation of cell migration, proliferation and numerous essential signaling pathways. Expectedly, we observed that optimized concentrations of NA, 3.5 mM and 7.0 mM, detached U251 from culturing petri dishes. Moreover, 7.0 mM of NA was capable of disrupting the leading-edge assembly. Additionally, we collected paraffin specimens from 85 GBM patients and evaluated the expression pattern of paxillin. Notably, we found that discernable paxillin signals were detected in 67 out of 85 samples. Given that leading edge is critical for cancer cell migration, we propose that NA treatment may be developed into a potential therapy for malignant glioma.

Insights

Nicotinic acid (NA) shows promise in treating malignant glioma by disassembling F-actin stress fibers crucial for cancer cell migration. This discovery offers a potential new therapeutic strategy for glioblastoma multiforme (GBM).

Area of Science:

Oncology
Cell Biology
Biochemistry

Background:

Malignant glioma, particularly glioblastoma multiforme (GBM), is a fatal brain tumor with poor prognosis due to rapid, diffuse invasion.
Cancer cell infiltration is a major obstacle for existing glioblastoma multiforme (GBM) therapies.
F-actin stress fibers are essential for cancer cell migration, proliferation, and signaling pathways, making them a potential therapeutic target.

Purpose of the Study:

To investigate the potential of nicotinic acid (NA) as a therapeutic agent for malignant glioma.
To explore the effect of nicotinic acid (NA) on F-actin stress fibers in glioblastoma multiforme (GBM) cells.
To evaluate the expression of paxillin in patient-derived glioblastoma multiforme (GBM) samples.

Main Methods:

Treatment of HEK293 and NIH3T3 cells with nicotinic acid (NA) to observe F-actin stress fiber disassembly.
Application of optimized nicotinic acid (NA) concentrations (3.5 mM and 7.0 mM) to U251 glioblastoma multiforme (GBM) cells.
Analysis of F-actin stress fiber disassembly and leading-edge disruption in glioblastoma multiforme (GBM) cells.
Immunohistochemical evaluation of paxillin expression in 85 glioblastoma multiforme (GBM) patient paraffin-embedded specimens.

Main Results:

Nicotinic acid (NA) treatment led to significant disassembly of F-actin stress fibers in non-cancerous cell lines.
Optimized concentrations of nicotinic acid (NA) (3.5 mM and 7.0 mM) detached U251 glioblastoma multiforme (GBM) cells from culture dishes.
7.0 mM nicotinic acid (NA) effectively disrupted the leading-edge assembly in glioblastoma multiforme (GBM) cells.
Paxillin expression was detected in 67 out of 85 (approximately 79%) glioblastoma multiforme (GBM) patient samples.

Conclusions:

Nicotinic acid (NA) demonstrates a novel function in targeting F-actin stress fibers, impacting cancer cell detachment and leading-edge disruption.
The findings suggest that nicotinic acid (NA) could be a potential therapeutic agent for malignant glioma.
Paxillin expression in a majority of glioblastoma multiforme (GBM) samples warrants further investigation in conjunction with nicotinic acid (NA) therapy.

Read full analysis

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