Role of Epigenetics for the Efficacy of Cisplatin

Lumpp, Tatjana; Stößer, Sandra; Fischer, Franziska; Hartwig, Andrea; Köberle, Beate

doi:10.3390/ijms25021130

Cited by 5 publications

(3 citation statements)

References 164 publications

(258 reference statements)

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“…lncRNA interacts with different miRNAs contributing to poor response to CDDP. [134] Figure 9 demonstrates the possible epigenetic mechanisms involved in acquired CDDP resistance and hence, regulation of these may promote CDDP sensitivity for better therapeutic outcome.…”

Section: Epigenetic Regulationmentioning

confidence: 99%

“…Based on these findings, methylation-induced of the S100P gene silencing may play a role in the development of acquired CDDP resistance. [142] [135,136,137,134]…”

Section: Epigenetic Regulationmentioning

confidence: 99%

“…Selected epigenetic mechanisms associated with CDDP resistance. BRCA1: Breast cancer gene 1; DSC3: Desmocollin 3; DNMTs: DNA Methyltransferases; FOX01: Forkhead box protein O1; H3 K27: Histone H3 at lysine 27; H3K36: Histone H3 at lysine 36; H3K4: Histone H3 at lysine 4; H3K56: Histone H3 at lysine 56; H3K79: Histone H3 at lysine 79; H3K9: Histone H3 at lysine 9; H3R17: Histone H3 at arginine 17; H3R26: Histone H3 at arginine 26; H3R8: Histone H3 at arginine 8; H4K5: Histone H4 at lysine 5, H4K12: Histone H4 at lysine 12; HIN1: Harpin-induced 1; HMTs: Histone Methyltransferases; HDACs: Histone deacetylases; HIF: Hypoxia-Inducible Factor; IGF: insulin-like growth factor; MASPIN: mammary serine protease inhibitor; MCJ: Methylationcontrolled J protein; MYLK3: Myosin Light Chain Kinase 3; p16: cyclin-dependent kinase inhibitor 2 A; p53: tumor protein 53; p73: p53 related protein; PAX5 -Paired box protein; PTEN: Phosphatase and TENsin homolog; RASSF1: Ras association domain family member 1; SFN: stratifin; TSG: Tumor suppressor genes [135,136,137,134].…”

mentioning

confidence: 99%

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Cisplatin Resistance in Cancer Therapy: Causes and Overcoming Strategies

Shruthi,

Bhasker Shenoy

2024

ChemistrySelect

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Dr. S. Shruthi, Prof. Dr. K. Bhasker Shenoy. Cisplatin (CDDP) is the first metal‐based drug and has been a popular drug in the treatment of various types of cancer for decades. Cancer cell death is promoted by this platinum‐based drug by generating DNA adducts and activating apoptotic signaling pathways. The development of drug resistance is the foremost clinical concern that compromises its efficacy. The mechanism of CDDP resistance encompasses changes in drug influx and efflux, drug accumulation reduction, enhanced drug detoxification, and repair which may affect its therapeutic value. Researchers have paid significant attention to overcoming CDDP resistance, which provides an opportunity to enhance clinical outcomes. Combinational therapy, use of CDDP analogs, phytochemicals, nanoparticle‐mediated drug delivery, gene targeting and regulation of drug induced epigenetic changes are the specific regimens to overcome CDDP resistance and treatment burden. In this review, we summarize the mechanisms involved in CDDP resistance and strategies considered to overcome these hurdles concerning preclinical and clinical studies. This may provide insights into the further development of novel approaches to uproot CDDP resistance, to ascertain a safer and more effective cancer therapy.

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Section: Epigenetic Regulationmentioning

confidence: 99%

“…Based on these findings, methylation-induced of the S100P gene silencing may play a role in the development of acquired CDDP resistance. [142] [135,136,137,134]…”

Section: Epigenetic Regulationmentioning

confidence: 99%

mentioning

confidence: 99%

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Cisplatin Resistance in Cancer Therapy: Causes and Overcoming Strategies

Shruthi,

Bhasker Shenoy

2024

ChemistrySelect

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Ubiquitin-specific proteases: From biological functions to potential therapeutic applications in gastric cancer

Li,

Bai,

et al. 2024

Biomedicine & Pharmacotherapy

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Strategies to enhance the response of liver cancer to pharmacological treatments

Marin,

Macias,

Asensio

et al. 2024

American Journal of Physiology-Cell Physiology

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In contrast to other types of cancers, there is no available efficient pharmacological treatment to improve the outcomes of patients suffering from major primary liver cancers, i.e., hepatocellular carcinoma and cholangiocarcinoma. This dismal situation is partly due to the existence in these tumors of many different and synergistic mechanisms of resistance, accounting for the lack of response of these patients, not only to classical chemotherapy but also to more modern pharmacological agents based on the inhibition of tyrosine kinase receptors (TKIs) and the stimulation of the immune response against the tumor using immune checkpoint inhibitors (ICIs). This review summarizes the effort to develop strategies to overcome this severe limitation, including searching for novel drugs derived from synthetic, semisynthetic, or natural products with vectorial properties against therapeutic targets to increase drug uptake or reduce drug export from cancer cells. Besides, immunotherapy is a promising line of research that is already starting to be implemented in clinical practice. Although less successful than in other cancers, the foreseen future for this strategy in treating liver cancers is considerable. Similarly, the pharmacological inhibition of epigenetic targets is highly promising. Many novel "epidrugs", able to act on "writer", "reader" and "eraser" epigenetic players, are currently being evaluated in preclinical and clinical studies. Finally, gene therapy is a broad field of research in the fight against liver cancer chemoresistance, based on the impressive advances recently achieved in gene manipulation. In sum, although the present is still dismal, there is reason for hope in the non-too-distant future.

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Role of Epigenetics for the Efficacy of Cisplatin

Cited by 5 publications

References 164 publications

Cisplatin Resistance in Cancer Therapy: Causes and Overcoming Strategies

Cisplatin Resistance in Cancer Therapy: Causes and Overcoming Strategies

Ubiquitin-specific proteases: From biological functions to potential therapeutic applications in gastric cancer

Strategies to enhance the response of liver cancer to pharmacological treatments

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