scholarly journals A Potential Role of RUNX2- RUNT Domain in Modulating the Expression of Genes Involved in Bone Metastases: An In Vitro Study with Melanoma Cells

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 751
Author(s):  
Michela Deiana ◽  
Luca Dalle Carbonare ◽  
Michela Serena ◽  
Samuele Cheri ◽  
Simona Mutascio ◽  
...  
Keyword(s):  
Bone Metastasis ◽  
Bone Metastases ◽  
Skeletal Development ◽  
Ectopic Expression ◽  
In Vitro Study ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Runt Domain ◽  
And Migration

Ectopic expression of RUNX2 has been reported in several tumors. In melanoma cells, the RUNT domain of RUNX2 increases cell proliferation and migration. Due to the strong link between RUNX2 and skeletal development, we hypothesized that the RUNT domain may be involved in the modulation of mechanisms associated with melanoma bone metastasis. Therefore, we evaluated the expression of metastatic targets in wild type (WT) and RUNT KO melanoma cells by array and real-time PCR analyses. Western blot, ELISA, immunofluorescence, migration and invasion ability assays were also performed. Our findings showed that the expression levels of bone sialoprotein (BSP) and osteopontin (SPP1) genes, which are involved in malignancy-induced hypercalcemia, were reduced in RUNT KO cells. In addition, released PTHrP levels were lower in RUNT KO cells than in WT cells. The RUNT domain also contributes to increased osteotropism and bone invasion in melanoma cells. Importantly, we found that the ERK/p-ERK and AKT/p-AKT pathways are involved in RUNT-promoted bone metastases. On the basis of our findings, we concluded that the RUNX2 RUNT domain is involved in the mechanisms promoting bone metastasis of melanoma cells via complex interactions between multiple players involved in bone remodeling.

scholarly journals LncRNA BANCR Facilitates Melanoma Cells Growth, Migration and Invasion by Inhibiting miR-206 and miR-571 to Induce G6PD Expression

2020 ◽  
Author(s):  
Yuye Yang ◽  
Huixin Yang ◽  
Zihan Yi ◽  
Lijuan Yang ◽  
Yueli Ni ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Nude Mice ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Mice Model ◽  
Nude Mice Model ◽  
And Migration

Abstract Background Here, we evaluated the roles of LncRNA BANCR in facilitating melanoma cells growth, migration, invasion. Moreover, we examined the molecular mechanisms of BANCR in promoting melanoma development.Methods Here, we measured BANCR expression by quantitative PCR. By transwell assay, we detected the cancer cell migration and invasion. The melanoma growth and migration induced by BANCR was detected by colony formation assay and in xenograft nude mice model. By Western blotting and luciferase assay, we evaluated the molecular mechanism of BANCR in inhibiting miR-206 and miR-571 to induce G6PD expression. Results We found BANCR was overexpressed in melanoma cells and tissues. In addition, we showed that BANCR promoted melanoma cells growth in vitro and in vivo. Moreover, BANCR promotes cancer cell migration and invasion in vitro, and induced melanoma metastasis in nude mice model. The migration and invasion induced by BANCR in melanoma cells were involved in upregulation of matrix metalloproteinases (MMPs) MMP2 and MMP9. Mechanismly, we indicated BANCR promoted melanoma cell growth and migration by suppressing miR-206 and miR-571 expression to activate glucose metabolism pathway and induce G6PD expression. Furthermore, miR-206 and miR-571 inhibited G6PD expression by directly binding the 3’UTR of G6PD. We also showed miR-206 and miR-571 inhibited the proliferation of melanoma cells.Conclusion Our findings indicated that BANCR contributed to melanoma development, which might provide novel insights into the function of lncRNA-driven carcinogenesis in melanoma.

scholarly journals Targeting Tumor Microenvironment: Metformin Suppresses IL-22 Induced Hepatocellular Carcinoma by Upregulating Hippo Signalling Pathway.

2020 ◽  
Author(s):  
Dong Zhao ◽  
Tao Zhou ◽  
Yi Luo ◽  
Chenchen Wang ◽  
Dongwei Xu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Signaling Pathway ◽  
Ectopic Expression ◽  
Tumor Development ◽  
In Vitro Study ◽  
Migration And Invasion ◽  
Hippo Signaling ◽  
Hippo Signaling Pathway

Abstract Background: Epidemiological studies have shown direct associations between type 2 diabetes and the risk of cancers. Accumulating evidence indicates that metformin is profoundly implicated in preventing tumor development. However, the exact mechanism underlying the anti-tumor effects of metformin in hepatocellular carcinoma (HCC) is still not clear. Methods: In this study, we investigated the effects of metformin on a mouse hepatocellular carcinoma (HCC) model and interleukin-22 (IL-22)-associated carcinogenesis in vitro. Results: We found that metformin significantly suppressed the incidence and tumor burden of HCC in the diethyl-nitrosamine (DEN)-induced HCC mouse model. As expected, expression of IL-22, an important factor involved in HCC progression, was markedly reduced by metformin. Treatment of HCC cells with metformin inhibited IL-22 induced cell proliferation, migration and invasion, and promoted cell apoptosis. Furthermore, ectopic expression of IL-22 makes HCC more aggressive whereas metformin largely compromised it in vitro and in vivo. Mechanistically, the whole transcriptome analysis and functional analysis revealed that Hippo signaling pathway was involved in the anti-tumor ability of metformin. Consistent with this, metformin directly activated Mst1/2, phosphorylated YAP1 in vitro. After blocking Hippo pathway by XMU-MP-1, the inhibitor of MST1/2, the inhibitory effects by metformin were dramatically attenuated as shown by in vitro study. Conclusions: Collectively, our findings illuminate a new regulatory mechanism, metformin activates Hippo signaling pathway to regulate IL-22 mediated HCC progression and provide new insights into its tumor-suppressive roles.

scholarly journals Loss of PR55α promotes proliferation and metastasis by activating MAPK/AKT signaling in hepatocellular carcinoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
JiangSheng Zhao ◽  
GuoFeng Chen ◽  
Jingqi Li ◽  
Shiqi Liu ◽  
Quan Jin ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle Progression ◽  
Lung Metastases ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Signal Pathways ◽  
And Migration ◽  
Healthy Liver

Abstract Background PR55α plays important roles in oncogenesis and progression of numerous malignancies. However, its role in hepatocellular carcinoma (HCC) is unclear. This study aims to characterize the functions of PR55α in HCC. Methods PR55α expressions in HCC tissues and paired healthy liver samples were evaluated using Western blot and tissue microarray immunohistochemistry. We knocked down the expression of PR55α in SMMC-7721 and LM3 cell lines via small interfering and lentivirus. In vitro cell counting, colony formation, migration and invasion assays were performed along with in vivo xenograft implantation and lung metastases experiments. The potential mechanisms involving target signal pathways were investigated by RNA-sequencing. Results PR55α expression level was suppressed in HCC tissues in comparison to healthy liver samples. Decreased PR55α levels were correlated with poorer prognosis (P = 0.0059). Knockdown of PR55α significantly promoted cell proliferation and migration, induced repression of the cell cycle progression and apoptosis in vitro while accelerating in vivo HCC growth and metastasis. Mechanistic analysis indicated that PR55α silencing was involved with MAPK/AKT signal pathway activation and resulted in increased phosphorylation of both AKT and ERK1/2. Conclusions This study identifies PR55α to be a candidate novel therapeutic target in the treatment of HCC.

Luteolin inhibits the proliferation, adhesion, migration and invasion of choroidal melanoma cells in vitro

2021 ◽  
pp. 108643
Author(s):  
Meng-Lin Shi ◽  
Yu-Fen Chen ◽  
Wei-Qi Wu ◽  
Yao Lai ◽  
Qi Jin ◽  
...  
Keyword(s):  
Choroidal Melanoma ◽  
Melanoma Cells ◽  
Migration And Invasion

Effect of targeted gold nanoparticles size on acoustic cavitation: An in vitro study on melanoma cells

Ultrasonics ◽  
2020 ◽  
Vol 102 ◽  
pp. 106061 ◽  
Author(s):  
Ahmad Shanei ◽  
Hadi Akbari-Zadeh ◽  
Neda Attaran ◽  
Mohammad Reza Salamat ◽  
Milad Baradaran-Ghahfarokhi
Keyword(s):  
Gold Nanoparticles ◽  
In Vitro Study ◽  
Acoustic Cavitation ◽  
Melanoma Cells ◽  
Vitro Study

IL-33/ST2 Axis Regulates Vasculogenic Mimicry via ERK1/2-MMP-2/9 Pathway in Melanoma

Dermatology ◽  
2019 ◽  
Vol 235 (3) ◽  
pp. 225-233 ◽  
Author(s):  
Fuhan Yang ◽  
Mingming Wen ◽  
Dayu Pan ◽  
Xian Lin ◽  
Jing Mo ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Vasculogenic Mimicry ◽  
Melanoma Cells ◽  
Tube Formation ◽  
Migration And Invasion ◽  
Rapid Progression ◽  
Inflammatory Factor ◽  
Action Methods ◽  
Significant Health

Background: Melanoma, an extremely malignant form of cancer, poses a significant health risk. Vasculogenic mimicry (VM), blood vessels formed by tumor cells instead of endothelial cells, is an important factor for the rapid progression of melanoma. Interleukin (IL)-33 is an inflammatory factor commonly found in the tumor microenvironment and plays an important role in the progression of many tumors. IL-33 acts on immune cells and tumor cells through its receptor ST2. This study hypothesized that IL-33 directly affects the progression of melanoma. Objectives: This study was designed to investigate the effect of IL-33 on VM of melanoma and its potential mechanism of action. Methods: The expression of ST2 was evaluated in 66 cases of melanoma collected from human patients, and the differences were analyzed. In vitro experiments were conducted to study the effects of the IL-33/ST2 axis on cell migration and invasion and to elucidate possible mechanisms. Results: ST2 expression is associated with that of matrix metalloproteinase (MMP)-2 and VM in melanoma of patients. IL-33 increases the abilities of proliferation, migration and invasion of melanoma cells and VM tube formation through ST2. IL-33 induces the production of MMP-2/9 via ERK1/2 phosphorylation. Conclusion: IL-33 can directly act on melanoma cells and promote its development.

scholarly journals PKA at a Cross-Road of Signaling Pathways Involved in the Regulation of Glioblastoma Migration and Invasion by the Neuropeptides VIP and PACAP

Cancers ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 123 ◽  
Author(s):  
Souheyla Bensalma ◽  
Soumaya Turpault ◽  
Annie-Claire Balandre ◽  
Madryssa De Boisvilliers ◽  
Afsaneh Gaillard ◽  
...  
Keyword(s):  
Rat Brain ◽  
Ex Vivo ◽  
Brain Parenchyma ◽  
Migration And Invasion ◽  
C6 Cells ◽  
Selective Inhibitors ◽  
Receptor System ◽  
And Migration ◽  
Vip Receptor

Glioblastoma (GBM) remains an incurable disease, mainly due to the high migration and invasion potency of GBM cells inside the brain. PI3K/Akt, Sonic Hedgehog (SHH), and PKA pathways play major regulatory roles in the progression of GBM. The vasoactive intestinal peptide (VIP) family of neuropeptides and their receptors, referred in this article as the “VIP-receptor system”, has been reported to regulate proliferation, differentiation, and migration in a number of tumor cell types and more particularly in GBM cells. These neuropeptides are potent activators of the cAMP/PKA pathway. The present study aimed to investigate the cross-talks between the above cited signaling cascades. Regulation by VIP-related neuropeptides of GBM migration and invasion was evaluated ex vivo in rat brain slices explanted in culture. Effects of different combinations of VIP-related neuropeptides and of pharmacological and siRNA inhibitors of PKA, Akt, and of the SHH/GLI1 pathways were tested on GBM migration rat C6 and human U87 GBM cell lines using the wound-healing technique. Quantification of nuclear GLI1, phospho-Akt, and phospho-PTEN was assessed by western-immunoblotting. The VIP-receptor system agonists VIP and PACAP-38 significantly reduced C6 cells invasion in the rat brain parenchyma ex vivo, and C6 and U87 migration in vitro. A VIP-receptor system antagonist, VIP10-28 increased C6 cell invasion in the rat brain parenchyma ex vivo, and C6 and migration in vitro. These effects on cell migration were abolished by selective inhibitors of the PI3K/Akt and of the SHH pathways. Furthermore, VIP and PACAP-38 reduced the expression of nuclear GLI1 while VIP10-28 increased this expression. Selective inhibitors of Akt and PKA abolished VIP, PACAP-38, and VIP10-28 effects on nuclear GLI1 expression in C6 cells. PACAP-38 induced a time-dependent inhibition of phospho-Akt expression and an increased phosphorylation of PTEN in C6 cells. All together, these data indicate that triggering the VIP-receptor system reduces migration and invasion in GBM cells through a PKA-dependent blockade of the PI3K/Akt and of the SHH/GLI1 pathways. Therefore, the VIP-receptor system displays anti-oncogenic properties in GBM cells and PKA is a central core in this process.

scholarly journals Effects of enamel matrix proteins on adherence, proliferation and migration of epithelial cells: A real-time in vitro study

2016 ◽  
Vol 13 (1) ◽  
pp. 160-168 ◽  
Author(s):  
Marzena Wyganowska-Swiatkowska ◽  
Paulina Urbaniak ◽  
Daniel Lipinski ◽  
Marlena Szalata ◽  
Karolina Borysiak ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Real Time ◽  
In Vitro Study ◽  
Vitro Study ◽  
Matrix Proteins ◽  
Enamel Matrix ◽  
Enamel Matrix Proteins ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Effects of Redox Modulation on Cell Proliferation, Viability, and Migration in Cultured Rat and Human Tendon Progenitor Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Yuk Wa Lee ◽  
Sai Chuen Fu ◽  
Man Yi Yeung ◽  
Chun Man Lawrence Lau ◽  
Kai Ming Chan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Vitamin C ◽  
Tendon Healing ◽  
In Vitro Study ◽  
Tendon Injury ◽  
Antioxidant Vitamin ◽  
Redox Modulation ◽  
And Migration

Tendon healing is slow and usually results in inferior fibrotic tissue formation. Recently, application of tendon derived stem cells (TDSCs) improved tendon healing in animal studies. In a chicken model, local injection of antioxidants reduced tendon adhesion after tendon injury. An in vitro study demonstrated that supplementation of H2O2reduced tenogenic marker expression in TDSCs. These findings suggested that the possibility of TDSCs is involved in tendon healing and the cellular activities of TDSCs might be affected by oxidative stress of the local environment. After tendon injury, oxidative stress is increased. Redox modulation might affect healing outcomes via affecting cellular activities in TDSCs. To study the effect of oxidative stress on TDSCs, the cellular activities of rat/human TDSCs were measured under different dosages of vitamin C or H2O2in this study. Lower dose of vitamin C increased cell proliferation, viability and migration; H2O2affected colony formation and suppressed cell migration, cell viability, apoptosis, and proliferation. Consistent with previous studies, oxidative stresses (H2O2) affect both recruitment and survival of TDSCs, while the antioxidant vitamin C may exert beneficial effects at low doses. In conclusion, redox modulation affected cellular activities of TDSCs and might be a potential strategy for tendon healing treatment.

Sign in / Sign up

Export Citation Format

Share Document