The Cross Talk between Cellular Senescence and Melanoma: From Molecular Pathogenesis to Target Therapies

Liu, Jiahua; Zheng, Runzi; Zhang, Yanghuan; Jia, Shuting; He, Yonghan; Liu, Jing

doi:10.3390/cancers15092640

Cited by 7 publications

(6 citation statements)

References 121 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In various tumour types including malignant melanoma, necroptotic mediators are strongly suppressed, indicating acquired necroptotic resistance of tumour cells [153]. In line with this, senescent melanocytes that are capable of resisting cell death, are emerging as a potential cell-of-origin in melanoma and specific targeting of factors released by senescent melanocytes are showing promise in counteracting melanoma [154,155]. In keratinocyte-derived tumours, such as head and neck SCC, a substantial amount of necroptosis has been reported and high levels of phosphorylated MLKL were shown to correlate with lymph node metastasis and tumour progression [156].…”

Section: Cell Death and Skin Tumour Formationmentioning

confidence: 89%

Cell death as an architect of adult skin stem cell niches

Lecomte,

Toniolo,

Hoste

2024

Cell Death Differ

View full text Add to dashboard Cite

Our skin provides a physical and immunological barrier against dehydration and environmental insults ranging from microbial attacks, toxins and UV irradiation to wounding. Proper functioning of the skin barrier largely depends on the interplay between keratinocytes- the epithelial cells of the skin- and immune cells. Two spatially distinct populations of keratinocyte stem cells (SCs) maintain the epidermal barrier function and the hair follicle. These SCs are inherently long-lived, but cell death can occur within their niches and impacts their functionality. The default cell death programme in skin is apoptosis, an orderly and non-inflammatory suicide programme. However, recent findings are shedding light on the significance of various modes of regulated necrotic cell death, which are lytic and can provoke inflammation within the local skin environment. While the presence of dying cells was generally regarded as a mere consequence of inflammation, findings in various human dermatological conditions and experimental mouse models of aberrant cell death control demonstrated that cell death programmes in keratinocytes (KCs) can drive skin inflammation and even tumour initiation. When cells die, they need to be removed by phagocytosis and KCs can function as non-professional phagocytes of apoptotic cells with important implications for their SC capacities. It is becoming apparent that in conditions of heightened SC activity, distinct cell death modalities differentially impact the different skin SC populations in their local niches. Here, we describe how regulated cell death modalities functionally affect epidermal SC niches along with their relevance to injury repair, inflammatory skin disorders and cancer.

show abstract

Section: Cell Death and Skin Tumour Formationmentioning

confidence: 89%

Cell death as an architect of adult skin stem cell niches

Lecomte,

Toniolo,

Hoste

2024

Cell Death Differ

View full text Add to dashboard Cite

show abstract

“…Like the CRGs discussed above, signaling pathways such as Cellular senescence and NF-kappa B signaling pathway are important mechanisms in melanoma. For example, studies have shown that the continuous accumulation of senescent melanocytes, fibroblasts, keratinocytes and immune cells in skin can promote melanoma pathogenesis and affect treatment, which is related to immune system aging [23]. Senescence inhibition therapy reduced tumor volumes and extended survival in a mouse melanoma model [23].…”

Section: Discussionmentioning

confidence: 99%

Identifying novel circadian rhythm biomarkers for diagnosis and prognosis of melanoma by an integrated bioinformatics and machine learning approach

Xu,

Zeng,

Bin

et al. 2024

Aging

View full text Add to dashboard Cite

Melanoma is a highly malignant skin tumor with poor prognosis. Circadian rhythm is closely related to melanoma pathogenesis. This study aimed to identify key circadian rhythm genes (CRGs) in melanoma and explore their potential as diagnostic and prognostic biomarkers. Microarray data of melanoma tissues and normal skins were obtained. Differentially expressed genes were identified and weighted gene co-expression network analysis (WGCNA) was performed to screen hub genes associated with melanoma. By overlapping hub genes with known CRGs, 125 melanoma-related CRGs were identified. Functional enrichment analysis revealed these CRGs were mainly involved in circadian rhythm and other cancer-related pathways. Three machine learning algorithms including LASSO regression, support vector machine-recursive feature elimination (SVM-RFE), and random forest were utilized to select key CRGs. Six CRGs (ABCC2, CA14, EGR3, FBXW7, LDHB, and PSEN2) were identified as key CRGs for melanoma diagnosis and prognosis. Diagnostic values of key CRGs were evaluated by ROC analysis in training and validation sets. Prognostic values of key CRGs were assessed by survival analysis and a multivariate Cox regression prognostic model was constructed. The prognostic model could effectively stratify melanoma patients into high- and low-risk groups with significantly different survival. A nomogram integrating clinical variables and risk score was built to predict 3-, 5- and 10-year overall survival of melanoma patients. In summary, six CRGs were identified as key genes associated with melanoma pathogenesis and may serve as promising diagnostic and prognostic biomarkers. The prognostic model and nomogram could facilitate personalized prognosis evaluation of melanoma patients.

show abstract

“…Increased lung cancerogenesis [203] More and more evidence points to the involvement of oxidative stress, which is brought on by high amounts of ROS, such as superoxide anions and hydrogen peroxide, in the development of melanoma [216,217]. When compared with nearby tissues or melanocytes, melanoma cells produce a lot of ROS, which they then excrete into extracellular space [218].…”

Section: Humansmentioning

confidence: 99%

Gender Differences in Oxidative Stress in Relation to Cancer Susceptibility and Survival

et al. 2023

View full text Add to dashboard Cite

Genetic, developmental, biochemical, and environmental variables interact intricately to produce sex differences. The significance of sex differences in cancer susceptibility is being clarified by numerous studies. Epidemiological research and cancer registries have revealed over the past few years that there are definite sex variations in cancer incidence, progression, and survival. However, oxidative stress and mitochondrial dysfunction also have a significant impact on the response to treatment of neoplastic diseases. Young women may be more protected from cancer than men because most of the proteins implicated in the regulation of redox state and mitochondrial function are under the control of sexual hormones. In this review, we describe how sexual hormones control the activity of antioxidant enzymes and mitochondria, as well as how they affect several neoplastic diseases. The molecular pathways that underlie the gender-related discrepancies in cancer that have been identified may be better understood, which may lead to more effective precision medicine and vital information on treatment options for both males and females with neoplastic illnesses.

show abstract

The Cross Talk between Cellular Senescence and Melanoma: From Molecular Pathogenesis to Target Therapies

Cited by 7 publications

References 121 publications

Cell death as an architect of adult skin stem cell niches

Cell death as an architect of adult skin stem cell niches

Identifying novel circadian rhythm biomarkers for diagnosis and prognosis of melanoma by an integrated bioinformatics and machine learning approach

Gender Differences in Oxidative Stress in Relation to Cancer Susceptibility and Survival

Contact Info

Product

Resources

About