Nck2 promotes human melanoma cell proliferation, migration and invasion in vitro and primary melanoma-derived tumor growth in vivo

Abstract Background In recent years, long non-coding RNAs (lncRNAs) are of great importance in development of different types of tumors, while the function of lncRNA ZFAS1 is rarely discussed in esophageal squamous cell carcinoma (ESCC). Therefore, we performed this study to explore the expression of exosomal lncRNA ZFAS1 and its molecular mechanism on ESCC progression. Methods Expression of ZFAS1 and miR-124 in ESCC tissues was detected. LncRNA ZFAS1 was silenced to detect its function in the biological functions of ESCC cells. A stable donor and recipient culture model was established. Eca109 cells transfected with overexpressed and low expressed ZFAS1 plasmid and miR-124 inhibitor labeled by Cy3 were the donor cells, and then co-cultured with recipient cells to observe the transmission of Cy3-ZFAS1 between donor cells and recipient cells. The changes of cell proliferation, apoptosis, invasion, and migration in recipient cells were detected. The in vivo experiment was conducted for verifying the in vitro results. Results LncRNA ZFAS1 was upregulated and miR-124 was down-regulated in ESCC tissues. Silencing of ZFAS1 contributed to suppressed proliferation, migration, invasion and tumor growth in vitro and induced apoptosis of ESCC cells. LncRNA ZFAS1 was considered to be a competing endogenous RNA to regulate miR-124, thereby elevating STAT3 expression. Exosomes shuttled ZFAS1 stimulated proliferation, migration and invasion of ESCC cells and restricted their apoptosis with increased STAT3 and declined miR-124. Furthermore, in vivo experiment suggested that elevated ZFAS1-exo promoted tumor growth in nude mice. Conclusion This study highlights that exosomal ZFAS1 promotes the proliferation, migration and invasion of ESCC cells and inhibits their apoptosis by upregulating STAT3 and downregulating miR-124, thereby resulting in the development of tumorigenesis of ESCC.

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The gangliosides as a possible molecular coupling factor between the proportion of radiosensitive cells in vitro and the metastatic potential in vivo within a human melanoma cell line

British Journal of Cancer ◽

10.1038/bjc.1997.115 ◽

1997 ◽

Vol 75 (5) ◽

pp. 639-649 ◽

Cited By ~ 11

Author(s):

CP Thomas ◽

A Buronfosse ◽

J Portoukalian ◽

B Fertil

Keyword(s):

Cell Line ◽

Melanoma Cell ◽

Melanoma Cell Line ◽

Metastatic Potential ◽

Coupling Factor ◽

Human Melanoma ◽

Human Melanoma Cell Line ◽

Human Melanoma Cell

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Excellent anti-proliferative and pro-apoptotic effects of (−)-epigallocatechin-3-gallate encapsulated in chitosan nanoparticles on human melanoma cell growth both in vitro and in vivo

Nanomedicine Nanotechnology Biology and Medicine ◽

10.1016/j.nano.2014.05.007 ◽

2014 ◽

Vol 10 (8) ◽

pp. 1619-1626 ◽

Cited By ~ 79

Author(s):

Imtiaz A. Siddiqui ◽

Dhruba J. Bharali ◽

Minakshi Nihal ◽

Vaqar M. Adhami ◽

Naghma Khan ◽

...

Keyword(s):

Cell Growth ◽

Melanoma Cell ◽

Chitosan Nanoparticles ◽

Human Melanoma ◽

Human Melanoma Cell ◽

Apoptotic Effects

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Modulation of human melanoma cell proliferation and apoptosis by hydatid cyst fluid of Echinococcus granulosus

OncoTargets and Therapy ◽

10.2147/ott.s146300 ◽

2018 ◽

Vol Volume 11 ◽

pp. 1447-1456 ◽

Cited By ~ 2

Author(s):

Xiang-Yang Gao ◽

Guang-Hui Zhang ◽

Li Huang

Keyword(s):

Cell Proliferation ◽

Hydatid Cyst ◽

Echinococcus Granulosus ◽

Melanoma Cell ◽

Human Melanoma ◽

Cyst Fluid ◽

Human Melanoma Cell ◽

Proliferation And Apoptosis ◽

Melanoma Cell Proliferation ◽

Hydatid Cyst Fluid

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Knockdown of microRNA-214-3p Promotes Tumor Growth and Epithelial-Mesenchymal Transition in Prostate Cancer

Cancers ◽

10.3390/cancers13235875 ◽

2021 ◽

Vol 13 (23) ◽

pp. 5875

Author(s):

Patrice Cagle ◽

Nikia Smith ◽

Timothy O. Adekoya ◽

Yahui Li ◽

Susy Kim ◽

...

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Tumor Growth ◽

Protein Tyrosine Kinase ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Oncogenic Signaling ◽

Mesenchymal Transition

Abnormal expression of microRNA miR-214-3p (miR-214) is associated with multiple cancers. In this study, we assessed the effects of CRISPR/Cas9 mediated miR-214 depletion in prostate cancer (PCa) cells and the underlying mechanisms. Knockdown of miR-214 promoted PCa cell proliferation, invasion, migration, epithelial-mesenchymal transition (EMT), and increased resistance to anoikis, a key feature of PCa cells that undergo metastasis. The reintroduction of miR-214 in miR-214 knockdown cells reversed these effects and significantly suppressed cell proliferation, migration, and invasion. These in vitro studies are consistent with the role of miR-214 as a tumor suppressor. Moreover, miR-214 knockout increased tumor growth in PCa xenografts in nude mice supporting its anti-oncogenic role in PCa. Knockdown of miR-214 increased the expression of its target protein, Protein Tyrosine Kinase 6 (PTK6), a kinase shown to promote oncogenic signaling and tumorigenesis in PCa. In addition, miR-214 modulated EMT as exhibited by differential regulation of E-Cadherin, N-Cadherin, and Vimentin both in vitro and in vivo. RNA-seq analysis of miR-214 knockdown cells revealed altered gene expression related to PCa tumor growth pathways, including EMT and metastasis. Collectively, our findings reveal that miR-214 is a key regulator of PCa oncogenesis and is a potential novel therapeutic target for the treatment of the disease.

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SUN-LB27 Interleukin-8 - a Possible Target for Melanoma Treatment? In-Vitro Studies Based on Human Melanoma Cell Models

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.2323 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Pandurangan Ramaraj

Keyword(s):

Cell Growth ◽

Melanoma Cell ◽

In Vitro Study ◽

Human Melanoma ◽

Human Melanoma Cell ◽

Melanoma Treatment ◽

Pre Treatment ◽

Melanoma Growth

Abstract Previous clinical studies showed that menstruating females were better protected in melanoma than post-menopausal women and men of any age. In addition, epidemiological studies showed an increased male mortality in melanoma. But these studies did not correlate with steroid status in females. Our in-vitro study showed female sex hormone progesterone significantly inhibited human melanoma cell growth. Further in-vitro study showed that progesterone action was mediated by a specific suppression of pro-inflammatory cytokine IL-8. Our research also showed that addition of IL-8 (1 ng/ml) to melanoma cells stimulated cell growth (117%) and suppression of IL-8 by curcumin (100 μM) pre-treatment suppressed human melanoma cell growth (26%) in-vitro. This observation prompted us to check the effect of male sex hormones androstenedione (AD) and testosterone (T) on melanoma cell growth. AD and T also suppressed cell growth and IL-8 secretion, but not as significantly as that of progesterone. However, addition of progesterone (10 μM) along with androgens showed an additive effect on the inhibition of melanoma cell growth and suppression of IL-8 secretion. As steroids (P, AD, T) targeted IL-8 for their action, it was decided to check whether vitamin-D3 also targeted IL-8 secretion and cell growth. Active form of vit-D3 (25 μM) also suppressed IL-8 secretion and cell growth. But, addition of progesterone (50 μM) along with D3 significantly suppressed cell growth and IL-8 secretion. This brought IL-8 into focus as a key molecule regulating melanoma cell growth. In order to check whether IL-8 was the molecule involved in regulating melanoma cell growth, IL-8 rescue experiment after curcumin (25 μM) pre-treatment was carried out. IL-8 (100 ng/ml) was able to rescue cell growth completely after pre-treatment with curcumin, suggesting IL-8 was the molecule involved in regulating melanoma cell growth. Literature also suggested important role for IL-8 in regulating melanoma cell growth. Conditional expression of IL-8 in nude mouse by Dr. Singh et al., indicated in-vivo role of IL-8 in melanoma growth and metastasis. Conclusion: Both, in-vitro and in-vivo studies suggested an important role for IL-8 in regulating melanoma growth and metastasis. So, IL-8 could be targeted to arrest melanoma growth and metastasis in-vivo. Hence, IL-8 could be a potential target for melanoma treatment.

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CircRNA CircCCT3 Acts as a Sponge of miR-613 to Promote Tumor Growth of Pancreatic Cancer Through Regulating VEGFA/VEGFR2 Signaling

10.21203/rs.3.rs-268983/v1 ◽

2021 ◽

Author(s):

Ji-Ping Hou ◽

Xue-Bo Men ◽

Lian-Ying Yang ◽

En-Kun Han ◽

Chun-Qi Han ◽

...

Keyword(s):

Cell Proliferation ◽

Tumor Growth ◽

Cell Lines ◽

Potential Interaction ◽

Migration And Invasion ◽

Promote Cell Proliferation ◽

Pathologic Features ◽

Vegfr2 Signaling

Abstract Objective This study was aimed at investigating the involvement of CircCCT3 in PC and study its interactions and functioning during the PC progression in vitro and in vivo by the use of molecular biology and bioinformatic methods.Methods The expressions of CircCCT3 and miR-613 in pancreatic carcinoma tissues and cell lines were evaluated by quantitative realtime PCR .The relationship between clinical pathologic features as well as survival rate and CircCCT3 expression was analyzed with Chi-square test and Kaplan–Meier method. CCK-8, wound healing , transwell assays and FITC-AnnexinV/PI assay were used to assess cell proliferation, migration, invasion and apoptosis after CircCCT3 overexpression or downregulation. Dual-Luciferase reporterassay, RNA immunoprecipitation (RIP) ,RNA pull down and fluorescence in situ hybridization(FISH) assays were performed to validate the potential interaction of CircCCT3, miR-613 and VEGFA.Nude mouse xenograft tumor assay was used to detect CircCCT3 effects on pancreatic tumorigenesis in vivo.Western blotting analysis was performed to examine the VEGFA and VEGFR2 protein expressions following.Results CircCCT3 expression was significantly increased in PC tissues and cell lines. CircCCT3 expression was negatively correlated with miR-613 expression. Moreover, it was found that CircCCT3 promote cell proliferation, migration, invasion and inhibited cell apoptosis in PC cells. CircCCT3 acted as a sponge for miR-613 to facilitate VEGFA and VEGFR2 expression. si-CirCCT3also inhibited tumor growth of PC in nude mice.si-CircCCT3 reduced VEGFA and VEGFR2 expression, whereas overexpression of CircCCT3 increased VEGFA and VEGFR2 expression.Conclusions Increased CircCCT3 suggests a poor prognosis in PC patients and promotes the migration and invasion through targeting VEGFA/VEGFR2 signaling. CircCCT3 may serve as a potential and promising therapeutic target for PC treatment.

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