Co-targeting of HMG-Co-A Reductase and Cycloxygenase-2 for the Treatment of Non-small Cell Lung Cancer

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Sharma Ashutosh; Ravi Kiran Ammu V.V.V.; Krishnamurthy Praveen T.

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Journal: Advanced Pharmaceutical Bulletin Year:2024 | Volume:14 | Issue:3 Page(s): 496-497

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Title

Co-targeting of HMG-Co-A Reductase and Cycloxygenase-2 for the Treatment of Non-small Cell Lung Cancer

Author(s)

Sharma Ashutosh | Ravi Kiran Ammu V.V.V. | Krishnamurthy Praveen T. | Issue Writer Certificate

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Abstract

To Editor, Non-small cell lung cancer (NSCLC) accounts for about 80-85% of total lung cancer cases with survival rate of <5 years, worldwide.1 The current therapeutic strategies for NSCLC include surgery, radiation therapy, chemotherapy and immunotherapy, limited due to their off-target side effects and patient incompliance.2 Among many cellular metabolic pathways, Mevalonate pathway is crucial metabolic process, due to its involvement in cellular energetics. HMG-Co-A reductase is a key enzyme which converts 3-hydroxy-3methylglutryl -CoA (HMG-Co-A) to mevalonate and further to farnesyl pyro-phosphate (FPP) geranylgeranyl pyro-phosphate (GGPP). HMG-CO-A expression has been associated with various cancers, such as breast, ovarian and colorectal cancer. Several studies have shown that high HMG-CO-A expression is associated with increased tumor progression and metastasis in clinical scenario. Moreover, inhibition of HMG-CO-A activity reduces the production of cholesterol and other isoprenoids which could affect their metabolic’s and starve the tumors. Statins have been reported to exert anti-tumoral effects by modulating cell proliferation, apoptosis, angiogenesis and metastasis. Therefore, HMGCO-A expression may serve as a potential therapeutic target in cancer. Inhibition of Mevalonate pathway by HMG-Co-A reductase inhibitors could help in blocking the cell cycle check points, resulting in blocking of NSCLC proliferation

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