IFI16 inhibits tumorigenicity and cell proliferation of bone and cartilage tumor cells

10.2741/2433 ◽  
2007 ◽  
Vol 12 (12) ◽  
pp. 4855 ◽  
Author(s):  
Yan Zhang
Keyword(s):  
Cell Proliferation ◽  
Tumor Cells ◽  
Cartilage Tumor ◽  
And Cartilage

scholarly journals Octreotide and Pasireotide Combination Treatment in Somatotroph Tumor Cells: Predominant Role of SST2 in Mediating Ligand Effects

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1816
Author(s):  
Jessica Amarù ◽  
Federica Barbieri ◽  
Marica Arvigo ◽  
Agnese Solari ◽  
Adriana Bajetto ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cells ◽  
Intracellular Signaling ◽  
Somatostatin Receptor ◽  
Combined Treatment ◽  
Primary Cultures ◽  
Receptor Subtype ◽  
Camp Accumulation ◽  
Gh Secretion ◽  
Somatostatin Receptor Ligands

First-generation somatostatin receptor ligands (fg-SRLs), such as octreotide (OCT), represent the first-line medical therapy in acromegaly. Fg-SRLs show a preferential binding affinity for somatostatin receptor subtype-2 (SST2), while the second-generation ligand, pasireotide (PAS), has high affinity for multiple SSTs (SST5 > SST2 > SST3 > SST1). Whether PAS acts via SST2 in somatotroph tumors, or through other SSTs (e.g., SST5), is a matter of debate. In this light, the combined treatment OCT+PAS could result in additive/synergistic effects. We evaluated the efficacy of OCT and PAS (alone and in combination) on growth hormone (GH) secretion in primary cultures from human somatotroph tumors, as well as on cell proliferation, intracellular signaling and receptor trafficking in the rat GH4C1 cell line. The results confirmed the superimposable efficacy of OCT and PAS in reducing GH secretion (primary cultures), cell proliferation, cAMP accumulation and intracellular [Ca2+] increase (GH4C1 cells), without any additive effect observed for OCT+PAS. In GH4C1 cells, co-incubation with a SST2-selective antagonist reversed the inhibitory effect of OCT and PAS on cell proliferation and cAMP accumulation, while both compounds resulted in a robust internalization of SST2 (but not SST5). In conclusion, OCT and PAS seem to act mainly through SST2 in somatotroph tumor cells in vitro, without inducing any additive/synergistic effect when tested in combination.

scholarly journals Contribution of the CK2 Catalytic Isoforms α and α’ to the Glycolytic Phenotype of Tumor Cells

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 181
Author(s):  
Francesca Zonta ◽  
Christian Borgo ◽  
Camila Paz Quezada Meza ◽  
Ionica Masgras ◽  
Andrea Rasola ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Therapeutic Strategies ◽  
The Other ◽  
Osteosarcoma Cell ◽  
Monomeric Form ◽  
New Information

CK2 is a Ser/Thr protein kinase overexpressed in many cancers. It is usually present in cells as a tetrameric enzyme, composed of two catalytic (α or α’) and two regulatory (β) subunits, but it is active also in its monomeric form, and the specific role of the different isoforms is largely unknown. CK2 phosphorylates several substrates related to the uncontrolled proliferation, motility, and survival of cancer cells. As a consequence, tumor cells are addicted to CK2, relying on its activity more than healthy cells for their life, and exploiting it for developing multiple oncological hallmarks. However, little is known about CK2 contribution to the metabolic rewiring of cancer cells. With this study we aimed at shedding some light on it, especially focusing on the CK2 role in the glycolytic onco-phenotype. By analyzing neuroblastoma and osteosarcoma cell lines depleted of either one (α) or the other (α’) CK2 catalytic subunit, we also aimed at disclosing possible pro-tumor functions which are specific of a CK2 isoform. Our results suggest that both CK2 α and α’ contribute to cell proliferation, survival and tumorigenicity. The analyzed metabolic features disclosed a role of CK2 in tumor metabolism, and suggest prominent functions for CK2 α isoform. Results were also confirmed by CK2 pharmacological inhibition. Overall, our study provides new information on the mechanism of cancer cells addiction to CK2 and on its isoform-specific functions, with fundamental implications for improving future therapeutic strategies based on CK2 targeting.

scholarly journals FGF9/FGFR2 increase cell proliferation by activating ERK 1/2, Rb/E2F1, and cell cycle pathways in mouse Leydig tumor cells

2018 ◽  
Vol 109 (11) ◽  
pp. 3503-3518 ◽  
Author(s):  
Ming‐Min Chang ◽  
Meng‐Shao Lai ◽  
Siou‐Ying Hong ◽  
Bo‐Syong Pan ◽  
Hsin Huang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Tumor Cells ◽  
Leydig Tumor Cells

scholarly journals Depsidones inhibit aromatase activity and tumor cell proliferation in a co-culture of human primary breast adipose fibroblasts and T47D breast tumor cells

2017 ◽  
Vol 4 ◽  
pp. 165-171 ◽  
Author(s):  
Suthat Chottanapund ◽  
M.B.M. Van Duursen ◽  
Anne Zwartsen ◽  
Supatchaya Timtavorn ◽  
Panida Navasumrit ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Breast Tumor ◽  
Aromatase Activity ◽  
Tumor Cell Proliferation ◽  
Breast Tumor Cells ◽  
Breast Adipose

scholarly journals Down-regulated LncR-MALAT1 suppressed cell proliferation and migration by inactivating autophagy in bladder cancer

RSC Advances ◽  
2018 ◽  
Vol 8 (54) ◽  
pp. 31019-31027
Author(s):  
Jiude Qi ◽  
Yanfeng Chu ◽  
Guangyan Zhang ◽  
Hongjun Li ◽  
Dongdong Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Lung Adenocarcinoma ◽  
Tumor Cells ◽  
Cell Proliferation And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Long non-coding RNA-metastasis-associated lung adenocarcinoma transcript (LncR-MALAT) is highly expressed in a variety of tumors, which can affect the progression of tumor cells.

Expression of heat-stable antigen on tumor cells provides co-stimulation for tumor-specific T cell proliferation and cytotoxicity in mice

1995 ◽  
Vol 25 (5) ◽  
pp. 1163-1167 ◽  
Author(s):  
Yi-Chong Wang ◽  
Lihua Zhu ◽  
Rebecca McHugh ◽  
Kenneth W. Sell ◽  
Periasamy Selvaraj
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Tumor Cells ◽  
T Cell Proliferation ◽  
Heat Stable ◽  
Heat Stable Antigen

scholarly journals Aberrant CD137 ligand expression induced by GATA6 overexpression promotes tumor progression in cutaneous T-cell lymphoma

Blood ◽  
2018 ◽  
Vol 132 (18) ◽  
pp. 1922-1935 ◽  
Author(s):  
Hiroaki Kamijo ◽  
Tomomitsu Miyagaki ◽  
Naomi Shishido-Takahashi ◽  
Rina Nakajima ◽  
Tomonori Oka ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tumor Cells ◽  
Cell Lymphoma ◽  
Cutaneous T Cell Lymphoma ◽  
Promote Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
Key Points ◽  
Ligand Expression ◽  
And Migration ◽  
Proliferation And Migration

Key Points Overexpression of GATA6 induces aberrant CD137L expression on tumor cells of CTCL. CD137-CD137L interactions promote cell proliferation and migration in CTCL cells, representing potential therapeutic targets.

scholarly journals CAFs affect the proliferation and treatment response of head and neck cancer spheroids during co-culturing in a unique in vitro model

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Mustafa Magan ◽  
Emilia Wiechec ◽  
Karin Roberg
Keyword(s):  
Cell Proliferation ◽  
Tumor Cell ◽  
Head And Neck ◽  
Treatment Response ◽  
Tumor Cells ◽  
In Vitro Model ◽  
Tumor Spheroids ◽  
Vitro Model ◽  
The Impact

Abstract Background Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous group of tumors for which the overall survival rate worldwide is around 60%. The tumor microenvironment, including cancer-associated fibroblasts (CAFs), is believed to affect the treatment response and migration of HNSCC. The aim of this study was to create a biologically relevant HNSCC in vitro model consisting of both tumor cells and CAFs cultured in 3D to establish predictive biomarkers for treatment response, as well as to investigate the impact of CAFs on phenotype, proliferation and treatment response in HNSCC cells. Methods Three different HNSCC patient-derived tumor cell lines were cultured with and without CAFs in a 3D model. Immunohistochemistry of the proliferation marker Ki67, epidermal growth factor receptor (EGFR) and fibronectin and a TUNEL-assay were performed to analyze the effect of CAFs on both tumor cell proliferation and response to cisplatin and cetuximab treatment in tumor spheroids (3D). mRNA expression of epithelial-mesenchymal transition (EMT) and cancer stem cells markers were analyzed using qRT-PCR. Results The results demonstrated increased cell proliferation within the tumor spheroids in the presence of CAFs, correlating with increased expression of EGFR. In spheroids with increased expression of EGFR, a potentiated response to cetuximab treatment was observed. Surprisingly, an increase in Ki67 expressing tumor cells were observed in spheroids treated with cisplatin for 3 days, correlating with increased expression of EGFR. Furthermore, tumor cells co-cultured with CAFs presented an increased EMT phenotype compared to tumor cells cultured alone in 3D. Conclusion Taken together, our results reveal increased cell proliferation and elevated expression of EGFR in HNSCC tumor spheroids in the presence of CAFs. These results, together with the altered EMT phenotype, may influence the response to cetuximab or cisplatin treatment.

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