Deciphering organellar damage associated cell death to overcome chemoresistance in lung cancer
Research Summary: Our study demonstrated that mitocurcumin induces paraptosis in NSCLC cells via ROS-JNK signaling, causing ER/mitochondrial stress and calcium uptake, offering a potential strategy to overcome chemoresistance in lung cancer treatment.
Researcher Spotlight
Girish Ch. Panigrahi is a PhD-Scholar at ACTREC, TMC. He is a passionate cancer researcher focusing on novel therapeutic strategy for the treatment of chemoresistant lung cancer and understanding the underlying mechanism of drug resistance.
Linkedin: https://in.linkedin.com/in/girish-panigrahi-5779b4202
Twitter: https://x.com/GirishPanigrah5
Instagram: https://www.instagram.com/girishch.panigrahi/
Lab: Dr. Vikram Gota, Advanced Centre for Treatment, Research & Education in Cancer (ACTREC)
Lab website: https://clinicalpharmacolo9.wixsite.com/department-of-clinic
What was the core problem you aimed to solve with this research?
Lung cancer remains the leading cancer type in terms of mortality worldwide. Chemoresistance is one of the major barriers for the treatment of lung cancer contributing to poor patient survival. Evading apoptosis is a key underlying mechanism for development of chemoresistance. We aimed to explore novel therapeutic strategies to overcome chemoresistance in lung cancer.
How did you go about solving this problem?
In this study, we have generated lung cancer resistant cells and utilized mitochondrial targeted curcumin (MitoC) to target therapy resistant lung cancer. To identify the underlying mechanism of mitoC induced cytotoxicity, we investigated differential gene expression upon MitoC treatment using whole exome sequencing and alteration in cell organellar ultrastructural by electron microscopy.
“Harnessing mitochondrial pathways offers a promising new approach to overcome therapy-resistant lung cancer.” — Dr. Vikram Gota
How would you explain your research outcomes (Key findings) to the non-scientific community?
Mitocurcumin induces ER/mitochondrial swelling in chemoresistant lung cancer cells. Transcriptomic profiling reveals upregulation of ER stress genes such as DDIT3, HSPA5, etc, which are known markers for paraptosis (Organellar stress associated cell death). Activation of ROS-mediated JNK signaling is one of the underlying mechanisms of mitoC induced paraptosis, which also induce mitochondrial calcium overload.
What are the potential implications of your findings for the field and society?
Our study highlights a novel avenue for addressing chemoresistance in lung cancer. Through global transcriptomic profiling and microscopic examination, we identified mitochondrial targeting as a critical mechanism that disrupts organelle architecture, triggers organellar stress-induced cell death, and offers potential therapeutic value in apoptosis-resistant tumors.
What was the exciting moment during your research?
The most standout scenario was observing the potential of a mitoC which drastically altered the ER and mitochondrial structure in chemoresistant lung cancer cells, highlighting the phenotypic effect of mitochondrial targeting to treat therapy resistant cancers.
Paper reference: Panigrahi, G.C., Joshi, A., Malhotra, D. et al. Mitocurcumin induces ROS-/JNK-mediated paraptosis to overcome chemoresistance in non-small cell lung cancer. Naunyn-Schmiedeberg’s Arch Pharmacol (2025). https://doi.org/10.1007/s00210-025-04852-y
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