scholarly journals PO-1000: Effect of X-rays and carbon ions on cell survival and expression of Hh pathway genes in cancer cells

2016 ◽  
Vol 119 ◽  
pp. S485
Author(s):  
K. Konings ◽  
M. Moreels ◽  
A. Suetens ◽  
A. Gonnissen ◽  
S. Isebaert ◽  
...  
Keyword(s):  
Cell Survival ◽  
Cancer Cells ◽  
X Rays ◽  
Carbon Ions

Hepatocyte Growth Factor Promotes Cell Survival by Phosphorylation of BAD in Gastric Cancer Cells

2008 ◽  
Vol 17 (1) ◽  
pp. 23-32 ◽  
Author(s):  
Kyung Hee Lee ◽  
Eun Young Choi ◽  
Min Kyoung Kim ◽  
Myung Soo Hyun ◽  
Jong Ryul Eun ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Survival ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Hepatocyte Growth

AMPA Receptor Antagonist CFM-2 Decreases Survivin Expression in Cancer Cells

2018 ◽  
Vol 18 (4) ◽  
pp. 591-596 ◽  
Author(s):  
Domingo Sanchez Ruiz ◽  
Hella Luksch ◽  
Marco Sifringer ◽  
Achim Temme ◽  
Christian Staufner ◽  
...  
Keyword(s):  
Cell Survival ◽  
Receptor Antagonist ◽  
Cancer Cells ◽  
Glutamate Receptors ◽  
Cancer Cell ◽  
Ampa Receptor ◽  
Ampa Receptors ◽  
Survivin Expression ◽  
Ampa Receptor Antagonist ◽  
Cancer Cell Survival

Background: Glutamate receptors are widely expressed in different types of cancer cells. α-Amino-3- hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors are ionotropic glutamate receptors which are coupled to intracellular signaling pathways that influence cancer cell survival, proliferation, and migration. Blockade of AMPA receptors by pharmacologic compounds may potentially constitute an effective tool in anticancer treatment strategies. Method: Here we investigated the impact of the AMPA receptor antagonist CFM-2 on the expression of the protein survivin, which is known to promote cancer cell survival and proliferation. We show that CFM-2 inhibits survivin expression at mRNA and protein levels and decreases the viability of cancer cells. Using a stably transfected cell line which overexpresses survivin, we demonstrate that over-expression of survivin enhances cancer cell viability and attenuates CFM-2–mediated inhibition of cancer cell growth. Result: These findings point towards suppression of survivin expression as a new mechanism contributing to anticancer effects of AMPA antagonists.

scholarly journals Differential Effects of Gold Nanoparticles and Ionizing Radiation on Cell Motility between Primary Human Colonic and Melanocytic Cells and Their Cancerous Counterparts

2021 ◽  
Vol 22 (3) ◽  
pp. 1418
Author(s):  
Elham Shahhoseini ◽  
Masao Nakayama ◽  
Terrence J. Piva ◽  
Moshi Geso
Keyword(s):  
Gold Nanoparticles ◽  
Ionizing Radiation ◽  
Cancer Cells ◽  
Cell Lines ◽  
Colorectal Adenocarcinoma ◽  
X Rays ◽  
Cell Adherence ◽  
Cancerous Cell ◽  
Primary Colon ◽  
Radiation Induced

This study examined the effects of gold nanoparticles (AuNPs) and/or ionizing radiation (IR) on the viability and motility of human primary colon epithelial (CCD841) and colorectal adenocarcinoma (SW48) cells as well as human primary epidermal melanocytes (HEM) and melanoma (MM418-C1) cells. AuNPs up to 4 mM had no effect on the viability of these cell lines. The viability of the cancer cells was ~60% following exposure to 5 Gy. Exposure to 5 Gy X-rays or 1 mM AuNPs showed the migration of the cancer cells ~85% that of untreated controls, while co-treatment with AuNPs and IR decreased migration to ~60%. In the non-cancerous cell lines gap closure was enhanced by ~15% following 1 mM AuNPs or 5 Gy treatment, while for co-treatment it was ~22% greater than that for the untreated controls. AuNPs had no effect on cell re-adhesion, while IR enhanced only the re-adhesion of the cancer cell lines but not their non-cancerous counterparts. The addition of AuNPs did not enhance cell adherence. This different reaction to AuNPs and IR in the cancer and normal cells can be attributed to radiation-induced adhesiveness and metabolic differences between tumour cells and their non-cancerous counterparts.

scholarly journals lincRNA-RP11400K9.4 Regulates Cell Survival and Migration of Breast Cancer Cells

2020 ◽  
Vol 17 (6) ◽  
pp. 769-779
Author(s):  
MIGUEL A. FERNÁNDEZ-ROJAS ◽  
JORGE MELENDEZ-ZAJGLA ◽  
VILMA MALDONADO LAGUNAS
Keyword(s):  
Breast Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
And Migration

scholarly journals Osteoblast-Derived Paracrine and Juxtacrine Signals Protect Disseminated Breast Cancer Cells from Stress

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1366
Author(s):  
Russell Hughes ◽  
Xinyue Chen ◽  
Natasha Cowley ◽  
Penelope D. Ottewell ◽  
Rhoda J. Hawkins ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cells ◽  
Metastatic Breast ◽  
Accessory Cell ◽  
Cancer Cell Survival

Metastatic breast cancer in bone is incurable and there is an urgent need to develop new therapeutic approaches to improve survival. Key to this is understanding the mechanisms governing cancer cell survival and growth in bone, which involves interplay between malignant and accessory cell types. Here, we performed a cellular and molecular comparison of the bone microenvironment in mouse models representing either metastatic indolence or growth, to identify mechanisms regulating cancer cell survival and fate. In vivo, we show that regardless of their fate, breast cancer cells in bone occupy niches rich in osteoblastic cells. As the number of osteoblasts in bone declines, so does the ability to sustain large numbers of breast cancer cells and support metastatic outgrowth. In vitro, osteoblasts protected breast cancer cells from death induced by cell stress and signaling via gap junctions was found to provide important juxtacrine protective mechanisms between osteoblasts and both MDA-MB-231 (TNBC) and MCF7 (ER+) breast cancer cells. Combined with mathematical modelling, these findings indicate that the fate of DTCs is not controlled through the association with specific vessel subtypes. Instead, numbers of osteoblasts dictate availability of protective niches which breast cancer cells can colonize prior to stimulation of metastatic outgrowth.

scholarly journals Radiation-induced HIF-1α cell survival pathway is inhibited by soy isoflavones in prostate cancer cells

2009 ◽  
Vol 124 (7) ◽  
pp. 1675-1684 ◽  
Author(s):  
Vinita Singh-Gupta ◽  
Hao Zhang ◽  
Sanjeev Banerjee ◽  
Dejuan Kong ◽  
Julian J. Raffoul ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Soy Isoflavones ◽  
Prostate Cancer Cells ◽  
Survival Pathway ◽  
Radiation Induced

scholarly journals Down-regulation of multiple cell survival proteins in head and neck cancer cells by an apoptogenic mutant of adenovirus type 5

Virology ◽  
2009 ◽  
Vol 392 (1) ◽  
pp. 62-72 ◽  
Author(s):  
S. Vijayalingam ◽  
T. Subramanian ◽  
Jan Ryerse ◽  
Mark Varvares ◽  
G. Chinnadurai
Keyword(s):  
Head And Neck Cancer ◽  
Cell Survival ◽  
Head And Neck ◽  
Cancer Cells ◽  
Neck Cancer ◽  
Adenovirus Type ◽  
Down Regulation ◽  
Multiple Cell ◽  
Adenovirus Type 5 ◽  
Survival Proteins

The role of hypoxia in endometrial cancer

2021 ◽  
Vol 22 ◽  
Author(s):  
Yarely M. Salinas-Vera ◽  
Dolores Gallardo-Rincón ◽  
Erika Ruíz-García ◽  
Macrina B. Silva-Cázares ◽  
Carmen Sol de la Peña-Cruz ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Targeted Therapies ◽  
Current Knowledge ◽  
Vasculogenic Mimicry ◽  
Cellular Processes ◽  
Corpus Uteri

: Endometrial cancer represents the most frequent neoplasia from the corpus uteri, and comprises the 14th leading cause of death in women worldwide. Risk factors that contribute to the disease include early menarche, late menopause, nulliparity, and menopausal hormone use, as well as hypertension and obesity comorbidities. The clinical effectiveness of chemotherapy is variable, suggesting that novel molecular targeted therapies against specific cellular processes associated with the maintenance of cancer cell survival and therapy resistance urged to ameliorate the rates of success in endometrial cancer treatment. In the course of tumor growth, cancer cells must adapt to decreased oxygen availability in the microenvironment by upregulation of hypoxia-inducible factors, which orchestrate the activation of a transcriptional program leading to cell survival. During this adaptative process, the hypoxic cancer cells may acquire invasive and metastatic properties as well as increased cell proliferation and resistance to chemotherapy, enhanced angiogenesis, vasculogenic mimicry, and maintenance of cancer cell stemness, which contribute to more aggressive cancer phenotypes. Several studies have shown that hypoxia-inducible factor 1 alpha (HIF-1α) protein is aberrantly overexpressed in many solid tumors from breast, prostate, ovarian, bladder, colon, brain, and pancreas. Thus, it has been considered an important therapeutic target. Here, we reviewed the current knowledge of the relevant roles of cellular hypoxia mechanisms and HIF-1α functions in diverse processes associated with endometrial cancer progression. In addition, we also summarize the role of microRNAs in the posttranscriptional regulation of protein-encoding genes involved in the hypoxia response in endometrial cancer. Finally, we pointed out the need for urgent targeted therapies to impair the cellular processes activated by hypoxia in the tumor microenvironment.

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