scholarly journals Green Synthesized Honokiol Transfersomes Relieve the Immunosuppressive and Stem-Like Cell Characteristics of the Aggressive B16F10 Melanoma

2021 ◽  
Vol Volume 16 ◽  
pp. 5693-5712
Author(s):  
Yasmeen Ezzeldeen ◽  
Shady Swidan ◽  
Aliaa ElMeshad ◽  
Aya Sebak
Keyword(s):  
2017 ◽  
Vol 46 (1) ◽  
pp. 34-38
Author(s):  
Hyang Suk Kim ◽  
Ji Min Cheon ◽  
Da Hye Kwon ◽  
Eun Ok Choi ◽  
Min Ju Kim ◽  
...  

2019 ◽  
Vol 26 (12) ◽  
pp. 910-918
Author(s):  
Kamal U. Zaidi ◽  
Firoz N. Khan ◽  
Sharique A. Ali ◽  
Kausar P. Khan

Background: Melanin plays a crucial role in camouflage, social communication and protection against harmful ultraviolet radiations. Melanin is synthesized by melanocytes through melanogenesis and several intrinsic and extrinsic factors are involved during the process. Any change occuring in the normal melanogenesis process can cause severe pigmentation problems of hypopigmentation or hyperpigmentation. Objective: The present study is based on the evaluation of the effect of thymoquinone on melanogenesis and their possible mechanism of action using the B16F10 melanoma cell line for the production via blocking signaling pathways. Methods: Phase contrast microscopy, cell viability, tyrosinase activity, melanin content and western blot analysis were used in the present study. Results: In the present investigation, cultured melanocytes exhibit that the stimulation of melanin synthesis when treated with thymoquinone. Tyrosinase activity and melanin production in B16F10 melanoma cell line was increased in doze-dependent manner. In western blot, we investigated the involvement of the cAMP/PKA pathway in thymoquinone induced melanogenesis. It was observed protein kinase inhibitors PKA, PKC, PKB and MEK1 decreased the stimulatory effects of thymoquinone from 11.45- fold value to 8.312, 6.631, 4.51, and 7.211-fold value, respectively. However, the results also prove that thymoquinone may partially induce tyrosinase expression via PKA, PKB, PKC and MEK1 signaling pathways. Conclusion: The present finding proposed that thymoquinone is a protective challenger for melanogenesis and it might be useful for the treatment of hypopigmentary disorders.


1988 ◽  
Vol 6 (2) ◽  
pp. 153-169 ◽  
Author(s):  
E. Barberá-Guillem ◽  
M. L. Cañavate ◽  
I. Lopez De Tejada ◽  
F. Vidal-Vanaclocha

2009 ◽  
Vol 23 (4) ◽  
pp. 558-567 ◽  
Author(s):  
M.Y. Tomiyoshi ◽  
M. Sakai ◽  
R.B. Baleeiro ◽  
D. Stankevicius ◽  
C.O. Massoco ◽  
...  

2008 ◽  
Vol 25 (6) ◽  
pp. 1463-1466 ◽  
Author(s):  
Eun-Suk Hong ◽  
Duc Thi Minh Nguyen ◽  
Dung Hoang Nguyen ◽  
Eun-Ki Kim

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 896
Author(s):  
Heejin Lim ◽  
Taewoo Yang ◽  
Wongeun Lee ◽  
Sung-Gyoo Park

There is growing evidence that myeloid-derived suppressor cells (MDSCs) are directly involved in all stages leading to metastasis. Many mechanisms for this effect have been proposed, but mechanisms of coregulation between tumor cells and MDSCs remain poorly understood. In this study, we demonstrate that MDSCs are a source of milk fat globule-epidermal growth factor (EGF) factor 8 (MFGE8), which is known to be involved in tumor metastasis. Interestingly, TGF-β, an abundant cytokine in the tumor microenvironment (TME), increased MFGE8 production by MDSCs. In addition, co-culturing MDSCs with B16F10 melanoma cells increased B16F10 cell migration, while MFGE8 neutralization decreased their migration. Taken together, these findings suggest that MFGE8 is an important effector molecule through which MDSCs promote tumor metastasis, and the TME positively regulates MFGE8 production by MDSCs through TGF-β.


1993 ◽  
Vol 104 (1) ◽  
pp. 31-36 ◽  
Author(s):  
C. de la Hoz ◽  
A. Baroja

The presence of high-ploidy cells in malignant tumours has long been documented. However, the biological significance of these cells is not known and there is a great deal of controversy over their proliferative potential. We have analysed the behaviour of these cells in two murine tumour lines, B16F10 melanoma and 3T3A31M angiosarcoma, determining their DNA content by microspectrophotometry and using time-lapse film studies. We have found a discrepancy between the presence of high-ploidy cells in metaphase and the absence of hyperploid telophases. High-ploidy metaphases may be aborted (mitotic polyploidization), prolonged in time or evolve in the form of multipolar, generally tripolar, mitoses. Our results suggest that high-ploidy cells are capable of proliferating, despite certain peculiarities in their cell cycle, and constitute a tumour subpopulation whose role in neoplasia merits further study.


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