scholarly journals S100A11 regulates renal carcinoma cell proliferation, invasion, and migration via the EGFR/Akt signaling pathway and E-cadherin

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770533 ◽  
Author(s):  
Lin Liu ◽  
Long Miao ◽  
Yang Liu ◽  
Aihua Qi ◽  
Ping Xie ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Renal Carcinoma ◽  
S100 Protein ◽  
Growth Factor Receptor ◽  
Carcinoma Cells ◽  
Cell Renal Cell Carcinoma ◽  
Invasion And Migration ◽  
And Migration ◽  
Renal Carcinoma Cells ◽  
E Cadherin

S100A11 is a S100 protein family member that contributes to cancer progression. Upregulated in human renal cancer tissues, S100A11 may be a prognostic marker for clear cell renal cell carcinoma, but how it functions in cancer is uncertain. Thus, we studied S100A11 and noted knockdown of S100A11 using short hairpin RNA, which inhibited proliferation, invasion, and migration of renal carcinoma cells as well as increased expression of E-cadherin and decreased expression of epidermal growth factor receptor/Akt in renal carcinoma cells. Therefore, S100A11 may be a key molecular target for treating renal carcinoma.

Effects of Epidermal Growth Factor Receptor Signal Pathway on Proliferation, Invasion and E-Cadherin/Vimentin Protein Expression in Laryngeal Carcinoma Hep-2 Cells

2021 ◽  
Vol 11 (8) ◽  
pp. 1595-1599
Author(s):  
Tingting Wu ◽  
Xuhong Zhou ◽  
Linfeng Ye ◽  
Shuang Li ◽  
Jing Huang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Invasion ◽  
Laryngeal Carcinoma ◽  
Growth Factor Receptor ◽  
Signal Pathway ◽  
Carcinoma Cells ◽  
Invasion And Migration ◽  
Epidermal Growth ◽  
And Migration ◽  
E Cadherin

Epidermal growth factor receptor (EGFR) is one transmembrane receptor with a high expression in more than 90% of head-neck squamous carcinoma cells. This study investigated the role of EGFR signal pathway on proliferation, invasion and expression of related proteins E-cadherin/Vimentin expression in laryngeal carcinoma cells. Laryngeal carcinoma Hep-2 cells were treated with EGFR agonist EGF or inhibitor Gefitinib followed by measuring cell cycle, proliferation index (PI) and apoptosis by flow cytometry. Transwell assay was employed for cell invasion and migration. Western blotting was further employed to test E-cadherin and Vimentin level. Compared to blank control group, EGF-treated cells had significantly lower S percentage of cell cycle at 6 h, 12 h and 24 h, plus higher PI. With prolonged incubation time, S ratio and PI were further significantly elevated, with more potent cell invasion and migration abilities, lower E-cadherin and Vimentin protein levels (p < 0.05). Gefitnib significantly elevated S ratio at 6 h, 12 h and 24 h cell cycle, reduced PI, invasion or migration ability, as upregulated E-cadherin and downregulated Vimentin protein (p < 0.05). Suppressing EGFR signal pathway could inhibit proliferation of laryngeal carcinoma cells, decrease cell invasion or migration, upregulate E-cadherin and downregulate Vimentin.

scholarly journals Cooperative Blockade of CK2 and ATM Kinases Drives Apoptosis in VHL-Deficient Renal Carcinoma Cells through ROS Overproduction

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 576
Author(s):  
Sofia Giacosa ◽  
Catherine Pillet ◽  
Irinka Séraudie ◽  
Laurent Guyon ◽  
Yann Wallez ◽  
...  
Keyword(s):  
High Throughput Screening ◽  
Renal Carcinoma ◽  
Kinase Inhibitors ◽  
Ex Vivo ◽  
Cancer Therapeutics ◽  
Carcinoma Cells ◽  
Wild Type ◽  
Cell Renal Cell Carcinoma ◽  
Von Hippel Lindau ◽  
Renal Carcinoma Cells

Kinase-targeted agents demonstrate antitumor activity in advanced metastatic clear cell renal cell carcinoma (ccRCC), which remains largely incurable. Integration of genomic approaches through small-molecules and genetically based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. The 786-O cell line represents a model for most ccRCC that have a loss of functional pVHL (von Hippel-Lindau). A multiplexed assay was used to study the cellular fitness of a panel of engineered ccRCC isogenic 786-O VHL− cell lines in response to a collection of targeted cancer therapeutics including kinase inhibitors, allowing the interrogation of over 2880 drug–gene pairs. Among diverse patterns of drug sensitivities, investigation of the mechanistic effect of one selected drug combination on tumor spheroids and ex vivo renal tumor slice cultures showed that VHL-defective ccRCC cells were more vulnerable to the combined inhibition of the CK2 and ATM kinases than wild-type VHL cells. Importantly, we found that HIF-2α acts as a key mediator that potentiates the response to combined CK2/ATM inhibition by triggering ROS-dependent apoptosis. Importantly, our findings reveal a selective killing of VHL-deficient renal carcinoma cells and provide a rationale for a mechanism-based use of combined CK2/ATM inhibitors for improved patient care in metastatic VHL-ccRCC.

scholarly journals Corilagin Represses Epithelial to Mesenchymal Transition Process Through Modulating Wnt/β-Catenin Signaling Cascade

Biomolecules ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1406 ◽  
Author(s):  
Sun Tae Hwang ◽  
Min Hee Yang ◽  
Alan Prem Kumar ◽  
Gautam Sethi ◽  
Kwang Seok Ahn
Keyword(s):  
Tumor Cells ◽  
Cancer Progression ◽  
Epithelial To Mesenchymal Transition ◽  
Transition Process ◽  
Carcinoma Cells ◽  
Signaling Cascade ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Anti Cancer ◽  
And Migration

Corilagin (CLG), a major component of several medicinal plants, can exhibit diverse pharmacological properties including those of anti-cancer, anti-inflammatory, and hepatoprotective qualities. However, there are no prior studies on its potential impact on the epithelial-to-mesenchymal transition (EMT) process. EMT can lead to dissemination of tumor cells into other organs and promote cancer progression. Hence, we aimed to investigate the effect of CLG on EMT and its mechanism(s) of action in tumor cells. We noted that CLG reduced the expression of various epithelial markers and up-regulated the expression of Occludin and E-cadherin in both basal and TGFβ-stimulated tumor cells. CLG treatment also abrogated cellular invasion and migration in colon and prostate carcinoma cells. In addition, CLG effectively attenuated the Wnt/β-catenin signaling cascade in TGFβ-stimulated cells. Overall, our study suggests that CLG may function as and effective modulator of EMT and metastasis in neoplastic cells.

scholarly journals mTORC2 mediate FLCN-induced HIF2α nuclear import and proliferation of clear cell renal cell carcinoma

2020 ◽  
Author(s):  
Xuyang Zhao ◽  
Yadong Ma ◽  
Jie Cui ◽  
Haiyang Zhao ◽  
Lei Liu ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Molecular Mechanism ◽  
Renal Cancer ◽  
Cancer Progression ◽  
Renal Cell ◽  
Clear Cell ◽  
Cell Renal Cell Carcinoma ◽  
Invasion And Migration ◽  
And Migration

AbstractClear cell renal cell carcinoma (ccRCC), as the most important type of renal carcinoma, has a high incidence and easy metastasis. Folliculin (FLCN) was identified as a tumor suppressor gene. Its deletions and mutations are associated with a potential risk of kidney cancer. At present, the specific molecular mechanism of FLCN-induced proliferation, invasion and migration in clear cell renal cell carcinoma remains elusive.In this study, we demonstrated that FLCN controled cell proliferation, invasion and migration through PI3K/mTORC2 pathway. FLCN combined with HIF2α in various normal and cancerous renal cells, and mTORC2 mediate FLCN effectively alleviated the deterioration of renal cancer cells by degrading HIF2α. Silencing of FLCN showed promotion of HIF2α protein expression, which in turn led to an increase in downstream target genes Cyclin D1 and MMP9. Moreover, when interfering with siFLCN, HIF2α degradation rate was delayed, and the time of entry into the nucleus was advanced. Taken together, our study illustrated that mTORC2 promoted the specific molecular mechanism of HIF2α by down-regulated FLCN, and might be a new therapeutic target against renal cancer progression.

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