Peroxisome disruption alters lipid metabolism and potentiates antitumor response with MAPK-targeted therapy in melanoma

Huang, Fan; Cai, Feiyang; Dahabieh, Michael S.; Gunawardena, Kshemaka; Talebi, Ali; Dehairs, Jonas; El-Turk, Farah; Park, Jae Yeon; Li, Mengqi; Goncalves, Christophe; Gagnon, Natascha; Su, Jie; LaPierre, Judith H.; Gaub, Perrine; Joyal, Jean-Sébastien; Mitchell, John J.; Swinnen, Johannes V.; Miller, Wilson H.; del Rincón, Sonia V.

doi:10.1172/jci166644

Cited by 9 publications

(1 citation statement)

References 56 publications

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“…Phosphorylated PINK1 participates in the regulation of mitosis by acting as a monomer ubiquitin kinase and a Parkin Ubl kinase [13]. Research shows that the downregulation of Myc weakens the transcriptional inhibition of PINK1, which induces PINK1 expression and regulates mitochondrial autophagy, thus promoting the production of a DTP state [14].…”

Section: Static State or Slow Proliferationmentioning

confidence: 99%

Diapause-like Drug-Tolerant Persister State: The Key to Nirvana Rebirth

Chen,

Jin

2024

Medicina

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Cancer is one of the leading causes of death in the world. Various drugs have been developed to eliminate it but to no avail because a tumor can go into dormancy to avoid therapy. In the past few decades, tumor dormancy has become a popular topic in cancer therapy. Recently, there has been an important breakthrough in the study of tumor dormancy. That is, cancer cells can enter a reversible drug-tolerant persister (DTP) state to avoid therapy, but no exact mechanism has been found. The study of the link between the DTP state and diapause seems to provide an opportunity for a correct understanding of the mechanism of the DTP state. Completely treating cancer and avoiding dormancy by targeting the expression of key genes in diapause are possible. This review delves into the characteristics of the DTP state and its connection with embryonic diapause, and possible treatment strategies are summarized. The authors believe that this review will promote the development of cancer therapy.

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Section: Static State or Slow Proliferationmentioning

confidence: 99%

Diapause-like Drug-Tolerant Persister State: The Key to Nirvana Rebirth

Chen,

Jin

2024

Medicina

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Transcriptional dysregulation and insights into clinical implications in melanoma

Shen,

Chen,

Nian

et al. 2024

Holist Integ Oncol

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Melanoma, a highly prevalent cancer worldwide, exhibits remarkable diversity and plasticity, with the adverse prognosis of advanced melanoma remaining a focal point of investigation. Despite the emergence of novel drugs and combination therapies improving patient outcomes, challenges such as drug resistance and incomplete mechanistic understanding persist. Transcriptional programs play a pivotal role in determining the characteristics of both normal and tumour cells, with their dysregulation of these programs being a hallmark of melanoma. Abnormalities in transcription regulation not only impact the characteristics of melanoma cells but also influence the tumor’s metabolism and immune microenvironment, forming a complex network in tumours. Thus, understanding these changes comprehensively is crucial for unravelling the mechanisms underlying melanoma initiation, progression, response to targeted and immune therapies, and treatment resistance. This review primarily explores the transcriptional features in normal melanocytes and melanoma cells, emphasizing their profound impact on cell metabolism and immune evasion. Furthermore, the plasticity of melanoma cells and its relationship with treatment resistance and metastasis are highlighted, emphasizing the importance of targeting dysregulated transcriptional factors and pathways. Finally, potential clinical implications in targeting transcriptional abnormalities are highlighted, particularly in metastatic or treatment-resistant melanomas. This comprehensive overview aims to contribute to the advancement of melanoma research and the development of precise and effective treatments.

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Drug-induced senescence by aurora kinase inhibitors attenuates innate immune response of macrophages on gastric cancer organoids

Yang,

Kwan,

et al. 2024

Cancer Letters

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Peroxisome disruption alters lipid metabolism and potentiates antitumor response with MAPK-targeted therapy in melanoma

Cited by 9 publications

References 56 publications

Diapause-like Drug-Tolerant Persister State: The Key to Nirvana Rebirth

Diapause-like Drug-Tolerant Persister State: The Key to Nirvana Rebirth

Transcriptional dysregulation and insights into clinical implications in melanoma

Drug-induced senescence by aurora kinase inhibitors attenuates innate immune response of macrophages on gastric cancer organoids

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