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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...

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Related Experiment Video

Updated: May 12, 2026

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

Cisplatin resistance associated with PARP hyperactivation.

Judith Michels¹, Ilio Vitale, Lorenzo Galluzzi

¹U848, INSERM, France.

Cancer Research

|April 5, 2013

Summary

Cisplatin-resistant cancer cells often show high PARP1 activity. Inhibiting PARP1 triggers DNA damage and apoptosis, making these cells susceptible to PARP inhibitors.

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Last Updated: May 12, 2026

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Tropomodulin 3 Overexpression as a Marker for Platinum Resistance and Immune Infiltration in Ovarian Cancer

Tropomodulin 3 Overexpression as a Marker for Platinum Resistance and Immune Infiltration in Ovarian Cancer

Published on: August 2, 2024

Area of Science:

Oncology
Molecular Biology
Cancer Research

Background:

Cisplatin (CDDP) is a common chemotherapy for non-small cell lung carcinoma, but resistance frequently develops.
Cancer cells can develop resistance to chemotherapy through various mechanisms, impacting treatment efficacy.
Poly(ADP-ribose) polymerase 1 (PARP1) is an enzyme involved in DNA repair and cellular stress responses.

Purpose of the Study:

To investigate the role of PARP1 in cisplatin-resistant cancer cells.
To determine if targeting PARP1 can overcome cisplatin resistance.
To evaluate the predictive value of PAR levels for PARP inhibitor response.

Main Methods:

Assessed PARP1 expression and activity in cisplatin-resistant cancer cells.
Treated cells and xenografts with PARP inhibitors and PARP1-targeting siRNAs.
Measured DNA damage response and apoptosis induction.
Correlated PAR levels and PARP1 expression with treatment response.

Main Results:

A majority of cisplatin-resistant cancer cells exhibited high PARP1 expression and activity.
PARP1 inhibition in resistant cells induced DNA damage and apoptosis via the intrinsic pathway.
Elevated poly(ADP-ribosyl)ated proteins (PAR) levels predicted response to PARP inhibitors.
PAR levels were a more accurate predictor of response than PARP1 expression alone.

Conclusions:

Cisplatin-resistant cancer cells often develop a dependency on PARP1.
PARP1 inhibition can re-sensitize resistant cancer cells to apoptosis.
PAR levels serve as a potential biomarker for predicting response to PARP inhibitors in resistant cancers.