Basic fibroblast growth factor promotes melanocyte migration via activating PI3K/Akt‐Rac1‐FAK‐JNK and ERK signaling pathways

Shi, Hongxue; Lin, Bin; Huang, Yan; Wu, Jiang; Zhang, Hongyu; Lin, Cai; Wang, Zhouguang; Zhu, Jingjing; Zhao, Yingzhen; Fu, Xiaobing; Lou, Zhencai; Li, Xiaokun; Xiao, Jian

doi:10.1002/iub.1531

Cited by 34 publications

(34 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, tumors in different locations may have alternate mechanisms of melanocyte colonization . We immunostained for several molecules that have been reported to affect melanocyte migration . We show that the receptor CD117 (c‐Kit) is expressed in a subset of the recurrent tumor's melanocytes and that its ligand, SCF (KITL), is diffusely expressed in the meningioma cells.…”

Section: Discussionmentioning

confidence: 90%

“…24 We immunostained for several molecules that have been reported to affect melanocyte migration. [17][18][19][20][21][22][23] We show that the receptor CD117 (c-Kit) is expressed in a subset of the recurrent tumor's melanocytes and that its ligand, SCF (KITL), is diffusely expressed in the meningioma cells. Also, bFGF is diffusely expressed in the recurrent tumor ( Fig.…”

Section: Discussionmentioning

confidence: 94%

“…There are several factors shown to stimulate normal melanocyte proliferation or migration. These include leukotriene C4 (LTC4), bFGF, SCF, endothelin‐1 (ET‐1), and stromal‐derived cell factor (SDF‐1) . There is also evidence that most of these factors (LTC4, bFGF, ET‐1, SDF‐1) are expressed by meningiomas, having a role in tumorigenesis and/or angiogenesis .…”

Section: Discussionmentioning

confidence: 99%

“…These include leukotriene C4 (LTC4), bFGF, SCF, endothelin-1 (ET-1), and stromal-derived cell factor (SDF-1). [17][18][19] There is also evidence that most of these factors (LTC4, bFGF, ET-1, SDF-1) are expressed by meningiomas, having a role in tumorigenesis and/or angiogenesis. [20][21][22][23] However, tumors in different locations may have alternate mechanisms of melanocyte colonization.…”

Section: Discussionmentioning

confidence: 99%

See 3 more Smart Citations

Clinicopathologic features and pathogenesis of melanocytic colonization in atypical meningioma

Harati

Magaki

et al. 2017

Neuropathology

View full text Add to dashboard Cite

Only two prior cases of benign dendritic melanocytes colonizing a meningioma have been reported. We add a third case, describe clinicopathologic features shared by the three, and elucidate the risk factors for this very rare phenomenon. A 29 year-old Hispanic woman presented with headache and hydrocephalus. MRI showed a lobulated enhancing pineal region mass measuring 41 mm in greatest dimension. Subtotal resection of the mass demonstrated an atypical meningioma, WHO grade II, and the patient subsequently underwent radiotherapy. She presented 4 years later with diplopia, and MRI showed an enhancing extra-axial mass measuring 47 mm in greatest dimension and centered on the tentorial incisura. Subtotal resection showed a brain-invasive atypical meningioma with melanocytic colonization. The previous two cases in the literature were atypical meningiomas, one of which was also brain invasive. Atypical meningiomas may be at particular risk for melanocytic colonization as they upregulate molecules known to be chemoattractants for melanocytes. We detected c-Kit expression in a minority of the melanocytes as well as stem cell factor and basic fibroblast growth factor in the meningioma cells, suggesting that mechanisms implicated in normal melanocyte migration may be involved. In some cases, brain invasion with disruption of the leptomeningeal barrier may also facilitate migration from the subarachnoid space into the tumor. Whether there is low-level proliferation of the dendritic melanocytes is unclear. Given that all three patients were non-Caucasian, meningiomas in persons and/or brain regions with increased dendritic melanocytes may predispose to colonization. The age range spanned from 6 years old to 70 years old. All three patients were female. The role of gender and estrogen in the pathogenesis of this entity remains to be clarified. Whether melanocytic colonization may also occur in the more common Grade I meningiomas awaits identification of additional cases.

show abstract

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Clinicopathologic features and pathogenesis of melanocytic colonization in atypical meningioma

Harati

Magaki

et al. 2017

Neuropathology

View full text Add to dashboard Cite

show abstract

“…VX-11e, an ERK2 inhibitor, inhibited the ERK2 activation in cervical carcinoma cells with either CKAP2 overexpression or not. FAK acts as a linker of transmembrane receptors with the major growth regulatory pathways, including extracellular signal-related kinase (ERK) and c-Jun-N-terminal kinase (JNK)/mitogen-activated protein kinase (MAPK) pathways 33 . Downregulating MMP-2/9 via inhibiting the activation of ERK/MAPK signaling pathways inhibited migration and invasion of colorectal cancer 34 .…”

Section: Discussionmentioning

confidence: 99%

Involvement of FAK-ERK2 signaling pathway in CKAP2-induced proliferation and motility in cervical carcinoma cell lines

Guo

Song

Hua

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Cervical carcinoma is the fourth most common cause of death in woman, caused by human papillomavirus (HPV) infections and arising from the cervix. Cytoskeleton-associated protein 2 (CKAP2), also known as tumor-associated microtubule-associated protein, has been linked to tumorigenic effects. In the present study, we screened CKAP2 as a new candidate gene which promotes development of cervical carcinoma, in two independent datasets (TCGA and GSE27678). Results showed that CKAP2 expression was significantly up-regulated in cervical cancerous tissues compared with normal counterparts. Gene set enrichment analysis (GSEA) showed that metastasis, cell cycle and FAK pathways were related with elevated CKAP2 expression. Knockdown of CKAP2 expression significantly inhibited cell proliferation, migration and invasion both in HeLa and C-33A cells. And depletion of CKAP2 down-regulated the expression of metastasis and cell cycle related proteins as well as the phosphorylation of ERK2 (p-ERK2), except E-cadherin. In vivo experiment revealed that knockdown of CKAP2 inhibited C-33A cells proliferation. However, FAK inhibitor PF-562271 and ERK2 inhibitor VX-11e treatment significantly inhibited CKAP2 overexpression-induced cell proliferation, migration and invasion in SiHa cells. In conclusion, our study suggests that CKAP2 acts as a functional oncogene in cervical carcinoma development and may exert its function by targeting FAK-ERK2 signaling pathway.

show abstract

Differentially expressed microRNAs in peripheral blood mononuclear cells of non‐segmental vitiligo and their clinical significance

Zhang

Yang

Liu

et al. 2020

Clinical Laboratory Analysis

View full text Add to dashboard Cite

Background Vitiligo is a frequent acquired depigmentation skin disease due to a loss of melanocytes. This study sought to characterize the expression pattern of microRNA (miRNA) in the peripheral blood mononuclear cells (PBMCs) of non‐segmental vitiligo (NSV) patients. We also screened for molecular markers that can be used to evaluate the clinical stages of NSV. Methods The miRNA expression profile in the PBMCs of four patients with progressive NSV and four healthy controls was determined using high‐throughput RNA sequencing. The divergently expressed miRNA was verified via qRT‐PCR in 26 progression, 26 stable NSV, and 26 healthy controls. Results Our findings posited that 323 miRNAs were differentially expressed in the PBMCs of NSV patients. The top 10 up‐regulated miRNAs in patients were hsa‐miR‐335‐5p, hsa‐miR‐20a‐5p, hsa‐miR‐514a‐3p, hsa‐miR‐144‐5p, hsa‐miR‐450b‐5p, hsa‐miR‐369‐3p, hsa‐miR‐101‐3p, hsa‐miR‐142‐5p, hsa‐miR‐19b‐3p, and hsa‐miR‐340‐5p. The top 10 down‐regulated miRNAs in patients were hsa‐miR‐4443, hsa‐miR‐1248, hsa‐miR‐6859‐3p, hsa‐miR‐668‐3p, hsa‐miR‐7704, hsa‐miR‐323a‐5p, hsa‐miR‐1237‐3p, hsa‐miR‐3127‐3p, hsa‐miR‐6735‐3p, and hsa‐miR‐127‐3p. The expressions of hsa‐miR‐20a‐5p in PBMCs of progressive and stable NSV were remarkably elevated relative to the healthy controls. In the characteristics curve analysis of hsa‐miR‐20a‐5p for differentiating progressive and stable NSV from normal subjects in PBMCs, the area under curve (AUC) was 0.92 and 0.81. Compared with patients in stable NSV, the hsa‐miR‐20a‐5p was markedly increased in PBMCs of progressive NSV patients, and the AUC was 0.81. Conclusion Our results showed that divergently expressed miRNAs contribute to the pathogenesis of NSV and that hsa‐miR‐20a‐5p can be applied as a biosignature for stage assessment in PBMCs of patients with NSV.

show abstract

Basic fibroblast growth factor promotes melanocyte migration via activating PI3K/Akt‐Rac1‐FAK‐JNK and ERK signaling pathways

Cited by 34 publications

References 63 publications

Clinicopathologic features and pathogenesis of melanocytic colonization in atypical meningioma

Clinicopathologic features and pathogenesis of melanocytic colonization in atypical meningioma

Involvement of FAK-ERK2 signaling pathway in CKAP2-induced proliferation and motility in cervical carcinoma cell lines

Differentially expressed microRNAs in peripheral blood mononuclear cells of non‐segmental vitiligo and their clinical significance

Contact Info

Product

Resources

About