Pigment Cell & Melanoma Research最新文献_第8页

The Lipid Droplet Protein DHRS3 Is a Regulator of Melanoma Cell State 脂滴蛋白 DHRS3 是黑色素瘤细胞状态的调控因子

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-31 DOI: 10.1111/pcmr.13208

Eleanor Johns, Yilun Ma, Pakavarin Louphrasitthiphol, Christopher Peralta, Miranda V. Hunter, Jeremy H. Raymond, Henrik Molina, Colin R. Goding, Richard M. White

{"title":"The Lipid Droplet Protein DHRS3 Is a Regulator of Melanoma Cell State","authors":"Eleanor Johns, Yilun Ma, Pakavarin Louphrasitthiphol, Christopher Peralta, Miranda V. Hunter, Jeremy H. Raymond, Henrik Molina, Colin R. Goding, Richard M. White","doi":"10.1111/pcmr.13208","DOIUrl":"10.1111/pcmr.13208","url":null,"abstract":"<div>\u0000 \u0000 Lipid droplets are fat storage organelles composed of a protein envelope and lipid-rich core. Regulation of this protein envelope underlies differential lipid droplet formation and function. In melanoma, lipid droplet formation has been linked to tumor progression and metastasis, but it is unknown whether lipid droplet proteins play a role. To address this, we performed proteomic analysis of the lipid droplet envelope in melanoma. We found that lipid droplet proteins were differentially enriched in distinct melanoma states; from melanocytic to undifferentiated. DHRS3, which converts all-trans-retinal to all-trans-retinol, is upregulated in the MITFLO/undifferentiated/neural crest-like melanoma cell state and reduced in the MITFHI/melanocytic state. Increased DHRS3 expression is sufficient to drive MITFHI/melanocytic cells to a more undifferentiated/invasive state. These changes are due to retinoic acid-mediated regulation of melanocytic genes. Our data demonstrate that melanoma cell state can be regulated by expression of lipid droplet proteins which affect downstream retinoid signaling.\u0000 </div>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142542417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

UVA Irradiation Promotes Melanoma Cell Proliferation Mediated by OPN3 Independently of ROS Production 紫外线照射促进黑色素瘤细胞增殖与 ROS 生成无关，由 OPN3 介导。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-30 DOI: 10.1111/pcmr.13206

Yulei Zhang, Wen Zeng, Wei Zhang, Yu Wang, Shuqi Jin, Ting Liu, Huanhuan Luo, Hongguang Lu

{"title":"UVA Irradiation Promotes Melanoma Cell Proliferation Mediated by OPN3 Independently of ROS Production","authors":"Yulei Zhang, Wen Zeng, Wei Zhang, Yu Wang, Shuqi Jin, Ting Liu, Huanhuan Luo, Hongguang Lu","doi":"10.1111/pcmr.13206","DOIUrl":"10.1111/pcmr.13206","url":null,"abstract":"UVA radiation, a primary risk factor in melanoma progression, partly acts through the mediation of reactive oxygen species (ROS). The role of ROS in driving cutaneous melanoma toward an invasive phenotype and whether it occurs through opsins (OPNs), which are photosensitive G protein-coupled receptors, is not fully understood. This study focuses on the impact of UVA radiation on melanoma cell proliferation, with a special emphasis on OPN3. Investigating the biphasic response to various UVA doses (0.75–9 J/cm2) in A375 and MV3 cell lines, and using EdU and CCK-8 assays, we observed dose-dependent changes in cell proliferation. Interestingly, UVA irradiation at these doses of 0.75, 1.5 and 3 J/cm2 did not significantly induce ROS production. Our study further delves into the role of OPN3, a photosensitive receptor, in melanoma progression. Following UVA exposure, an increase in OPN3 expression was observed in melanoma cells lines A375 and MV3, indicating its role as a UVA-sensitive sensor and its influence on cell proliferation. Additionally, UVA-induced calcium flux in two melanoma cells lines pointed to a calcium-dependent G protein-coupled pathway in melanoma proliferation, mediated by OPN3 and not reliant on ROS. This research sheds light on the mechanism of UVA-induced melanoma progression, underscoring OPN3 as a pivotal regulator and advancing our understanding of UVA's interaction with opsins in melanoma progression.","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142542418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bay 11-7082, an NF-κB Inhibitor, Prevents Post-Inflammatory Hyperpigmentation Through Inhibition of Inflammation and Melanogenesis NF-κB 抑制剂 Bay 11-7082 可通过抑制炎症和黑色素生成来预防炎症后色素沉着。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-27 DOI: 10.1111/pcmr.13207

Juwon Moon, Ik Jun Moon, Hoyong Hyun, Jae Min Yoo, Seung Hyun Bang, Youngsup Song, Sung Eun Chang

{"title":"Bay 11-7082, an NF-κB Inhibitor, Prevents Post-Inflammatory Hyperpigmentation Through Inhibition of Inflammation and Melanogenesis","authors":"Juwon Moon, Ik Jun Moon, Hoyong Hyun, Jae Min Yoo, Seung Hyun Bang, Youngsup Song, Sung Eun Chang","doi":"10.1111/pcmr.13207","DOIUrl":"10.1111/pcmr.13207","url":null,"abstract":"<div>\u0000 \u0000 Post-inflammatory hyperpigmentation (PIH) is a very common disorder of cutaneous hyperpigmentation, which poses a persistent management challenge in the fields of dermatology and esthetics. This study was designed to explore the anti-melanogenic and anti-inflammatory effects of Bay 11-7082, an NF-κB inhibitor, using small-molecule screening, to determine its potential application for PIH prevention. The molecular mechanisms were investigated in vitro and ex vivo in epidermis-humanized mice using melanin content, RT-PCR, and immunoblotting. Bay 11-7082 suppressed proinflammatory cytokines and ameliorated 2,4-dinitrofluorobenzene (DNFB)-induced contact dermatitis on day 15. The suppression of melanin synthesis by Bay 11-7082 was attributed to the reduction of MITF, which was induced by extracellular signal-regulated kinase activation. Bay 11-7082 reduced epidermal melanin accumulation in UVB-stimulated ex vivo human epidermis as well as in the ear and tail skin of K14-stem cell factor (SCF) transgenic mice. Topical administration of Bay 11-7082 improved PIH on day 35 in the post-DNFB dorsal skin of K14-SCF transgenic mice. In conclusion, Bay 11-7082 can be considered a promising candidate for the development of a preventive topical agent for PIH.\u0000 </div>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Low-Dose Baricitinib Plus Narrow-Band Ultraviolet B for the Treatment of Progressive Non-Segmental Vitiligo: A Prospective, Controlled, Open-Label Study 低剂量巴利替尼加窄带紫外线 B 治疗进展期非节段性白癜风：一项前瞻性、对照、开放标签研究。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-23 DOI: 10.1111/pcmr.13209

Zhonghui Hu, Lu Lu, Jindi Feng, Hongbin Song, Shiyu Zhang, Lu Yang, Yuehua Liu, Tao Wang

{"title":"Low-Dose Baricitinib Plus Narrow-Band Ultraviolet B for the Treatment of Progressive Non-Segmental Vitiligo: A Prospective, Controlled, Open-Label Study","authors":"Zhonghui Hu, Lu Lu, Jindi Feng, Hongbin Song, Shiyu Zhang, Lu Yang, Yuehua Liu, Tao Wang","doi":"10.1111/pcmr.13209","DOIUrl":"10.1111/pcmr.13209","url":null,"abstract":"Vitiligo is a chronic autoimmune disease, and current treatments for vitiligo have limited efficacy. Janus kinase (JAK) inhibitors could offer new therapeutic options. To evaluate the efficacy and safety of baricitinib, an oral JAK1/2 inhibitor, combined with narrow-band ultraviolet B (NB-UVB) in vitiligo treatment. This prospective, controlled, open-label study included adults with progressive non-segmental vitiligo (NSV). Patients were assigned to combination therapy with baricitinib 2 mg daily and NB-UVB three times a week or NB-UVB alone three times a week (control). The primary endpoint was the proportion of patients achieving 50% or greater improvement from baseline in the total Vitiligo Area Scoring Index (T-VASI50) at week 16. Of the 33 patients (mean age, 34.1 years; 27.3% women) who completed the study, 12 of 17 (70.6%) patients in the combination group and 2 of 16 (12.5%) in the control group had a T-VASI50 response at week 16 (relative risk [RR] = 5.6; 95% CI = 1.5–21.4; p = 0.001). Adverse events were minor, including erythema, mild blister after phototherapy and acne. Combination therapy with low-dose baricitinib and NB-UVB was effective and well tolerated in adults with progressive NSV.","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142491758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

25th Annual meeting of the European Society for Pigment Cell Research, Marseille, France 第 25 届欧洲色素细胞研究学会年会，法国马赛

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-14 DOI: 10.1111/pcmr.13192

引用次数: 0

PASPCR 2024 Annual Meeting, New York, NY PASPCR 2024 年年会，纽约州纽约市

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-14 DOI: 10.1111/pcmr.13191

引用次数: 0

Meeting Report From the 2023 Cure Ocular Melanoma (CURE OM) Global Science Meeting, Philadelphia, PA, November 2023 2023 年治疗眼部黑色素瘤（CURE OM）全球科学会议报告，宾夕法尼亚州费城，2023 年 11 月。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-09 DOI: 10.1111/pcmr.13205

Rino S. Seedor, Andrew E. Aplin, Corine Bertolotto, Richard D. Carvajal, Nigel Deacon, Katie Doble, Omid Hamid, Rizwan Haq, Miriam Kadosh, Shaheer Khan, Jacqueline Kraska, Jose Lutzky, Meredith McKean, Kamaneh Montazeri, Justin Moser, Michael Onken, Marlana Orloff, Joseph J. Sacco, Keiran Smalley, Sara M. Selig

引用次数: 0

Sex Differences in Acral Lentiginous Melanoma: A Retrospective Cohort Analysis of 3617 Cases From the Surveillance, Epidemiology, and End Results Database 口腔扁平状黑色素瘤的性别差异：对监测、流行病学和最终结果数据库中 3617 例病例的回顾性队列分析。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-10-01 DOI: 10.1111/pcmr.13200

Jennifer M. Fernandez, Mitchell A. Taylor, Katherine Plampton, Erin X. Wei, Ashley Wysong

引用次数: 0

LL37-DNA Complex Drives Vitiligo Progression Through TLR9-MyD88 Signaling Pathways LL37-DNA复合物通过TLR9-MyD88信号通路驱动白癜风进展

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-09-30 DOI: 10.1111/pcmr.13202

Jingying Wang, Hanxiao Mao, Rulan Liu, Ziyuan Zeng, Lvsha Xie, Yan Yang, Yuanmin He

{"title":"LL37-DNA Complex Drives Vitiligo Progression Through TLR9-MyD88 Signaling Pathways","authors":"Jingying Wang, Hanxiao Mao, Rulan Liu, Ziyuan Zeng, Lvsha Xie, Yan Yang, Yuanmin He","doi":"10.1111/pcmr.13202","DOIUrl":"10.1111/pcmr.13202","url":null,"abstract":"<div>\u0000 \u0000 Vitiligo is an autoimmune disorder characterized by chronic depigmentation and milk-white patches on the skin. Skin infiltration by autoreactive CD8+ T cells causes melanocyte destruction in vitiligo. Multiple risk factors, particularly immune-related inflammatory factors, are involved in the disappearance of melanocytes. LL37 is a classic damage-associated molecular pattern molecule that is involved in the development of various autoimmune diseases. An enhanced expression of LL37 in vitiligo is known; however, the exact role of LL37 in melanocyte loss has not yet been elucidated. In the present study, we detected increased LL37 expression in vitiligo serum and lesions. Furthermore, we confirmed that cultured keratinocytes released LL37 after treatment with H2O2. Moreover, the LL37-DNA complex enhanced the secretion of CXCL9, CXCL10, and CXCL16 from keratinocytes via the TLR9-MyD88 signaling pathway and facilitated the migration of CD8+ T cells. Altogether, our study demonstrates that LL37 released from keratinocytes binds to DNA and contributes to melanocyte destruction under oxidative stress-induced autoimmunity in vitiligo.\u0000 </div>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142338013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cholinergic Signaling Mediated by Muscarinic Receptors Triggers the Ultraviolet-Induced Release of Melanosome in Cultured Melanoma Cells 由毒蕈碱受体介导的胆碱能信号在培养的黑色素瘤细胞中触发紫外线诱导的黑色素体释放。

IF 3.9 3区医学

Pigment Cell & Melanoma Research Pub Date : 2024-09-30 DOI: 10.1111/pcmr.13201

Maggie Suisui Guo, Qiyun Wu, Yingjie Xia, Jiahui Wu, Xiaoyang Wang, Gary Ka Wing Yuen, Tina Tingxia Dong, Jin Gao, Karl Wah Keung Tsim

{"title":"Cholinergic Signaling Mediated by Muscarinic Receptors Triggers the Ultraviolet-Induced Release of Melanosome in Cultured Melanoma Cells","authors":"Maggie Suisui Guo, Qiyun Wu, Yingjie Xia, Jiahui Wu, Xiaoyang Wang, Gary Ka Wing Yuen, Tina Tingxia Dong, Jin Gao, Karl Wah Keung Tsim","doi":"10.1111/pcmr.13201","DOIUrl":"10.1111/pcmr.13201","url":null,"abstract":"In skin, melanin is synthesized and stored in melanosomes. In epidermal melanocytes, melanosomes are transported to and internalized by the neighboring keratinocytes, subsequently leading to skin pigmentation. Ultraviolet (UV) radiation induces the release of acetylcholine (ACh) from keratinocytes, which in turn activates ACh receptors (AChRs) on nearby melanocytes, forming a proposed “skin synapse”. Here, we illustrated that the UV-induced melanosome release from cultured B16F10 melanoma cells could be mediated by co-actions of ACh. In the cell cultures, UV exposure robustly elicited melanosome release. Applied bethanechol (BeCh), an agonist of muscarinic AChR (mAChR), could significantly enhance the release. In parallel, the intracellular Ca2+ mobilization was regulated. The applied antagonists of M1 and/or M3 mAChRs could block the UV-induced melanosome release and the mobilization of intracellular Ca2+. The phosphorylation of PKC, triggered by UV and BeCh treatments, could be suppressed by the applied mAChR antagonists. The expressions of tethering complex for exocytosis, for example, Sec8, Exo70, and Rab11b, as well as synaptotagmin, were increased under UV exposure together with mAChR agonist: The inductions were fully abolished by M1 or M3 antagonist. Here, we hypothesize that the cholinergic signaling is playing roles in UV-induced exocytosis of melanosomes.","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":"38 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142338012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0