JHDM1B expression regulates ribosome biogenesis and cancer cell growth in a p53 dependent manner

2014 ◽  
Vol 136 (5) ◽  
pp. E272-E281 ◽  
Author(s):  
Marianna Penzo ◽  
Lucia Casoli ◽  
Daniela Pollutri ◽  
Laura Sicuro ◽  
Claudio Ceccarelli ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cell ◽  
Ribosome Biogenesis ◽  
Dependent Manner ◽  
Cancer Cell Growth

Abstract 5145: KDM2B expression regulates ribosome biogenesis and cancer cell growth in a p53-dependent manner

2014 ◽  
Author(s):  
Marianna Penzo ◽  
Lucia Casoli ◽  
Laura Sicuro ◽  
Alice Galibiati ◽  
Daniela Pollutri ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cell ◽  
Ribosome Biogenesis ◽  
Dependent Manner ◽  
Cancer Cell Growth

scholarly journals LRH-1 drives colon cancer cell growth by repressing the expression of theCDKN1Agene in a p53-dependent manner

2015 ◽  
Vol 44 (2) ◽  
pp. 582-594 ◽  
Author(s):  
Holly B. Kramer ◽  
Chun-Fui Lai ◽  
Hetal Patel ◽  
Manikandan Periyasamy ◽  
Meng-Lay Lin ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Dependent Manner ◽  
Cancer Cell Growth

scholarly journals Qici Sanling Decoction Suppresses Glutamine Consumption and Bladder Cancer Cell Growth through Inhibiting c-Myc Expression

2022 ◽  
Vol 2022 ◽  
pp. 1-9
Author(s):  
Weihua Chen ◽  
Weifeng Wang ◽  
Jun Zhang ◽  
Guoqiang Liao ◽  
Jie Bai ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Alternative Therapy ◽  
Bladder Cancer Cell ◽  
Dependent Manner ◽  
Cancer Cell Growth ◽  
Protein Levels ◽  
T24 Cells ◽  
Glutamine Consumption

Traditional Chinese medicine (TCM) is widely used as an alternative therapy for cancer treatment in China. Glutamine catabolism plays an important role in cancer development. Qici Sanling decoction (QCSL) suppresses bladder cancer growth. However, the association between QCSL and glutamine catabolism remains unknown. In this study, different doses of QCSL were applied to T24 cells, followed by the measurements of cell viability and apoptosis using CCK-8 and Annexin V/PI assay, respectively. Furthermore, glutamine consumption was detected using the glutamine assay kit. QCSL was observed to inhibit cell growth and induced cell apoptosis in a dose-dependent manner. Analysis of glutamine consumption revealed that QCSL suppressed glutamine consumption in T24 cells. Furthermore, QCSL decreased the mRNA and protein levels of c-Myc, GLS1, and SLC1A5. All these effects induced by QCSL could be alleviated by c-Myc overexpression, indicating c-Myc was involved in the protective role of QCSL in bladder cancer. In addition, QCSL was found to inhibit tumor growth in the xenograft tumor model. The similar results were obtained in tumor samples that protein levels of c-Myc, GLS1, and SLC1A5 were decreased upon treatment with QCSL. In conclusion, QCSL suppresses glutamine consumption and bladder cancer cell growth through inhibiting c-Myc expression.

Fibroblasts Isolated from Common Sites of Breast Cancer Metastasis Enhance Cancer Cell Growth Rates and Invasiveness in an Interleukin-6–Dependent Manner

2008 ◽  
Vol 68 (21) ◽  
pp. 9087-9095 ◽  
Author(s):  
Adam W. Studebaker ◽  
Gianluca Storci ◽  
Jillian L. Werbeck ◽  
Pasquale Sansone ◽  
A. Kate Sasser ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Growth Rates ◽  
Interleukin 6 ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Dependent Manner ◽  
Cancer Cell Growth

1615 TADALAFIL INHIBITS PROSTATE CANCER CELL GROWTH IN A DOSE-DEPENDENT MANNER

2011 ◽  
Vol 185 (4S) ◽  
Author(s):  
Niels Johnsen ◽  
Limin Ma ◽  
Asim Abdel-Mageed ◽  
Wayne Hellstrom
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Dependent Manner ◽  
Cancer Cell Growth ◽  
Dose Dependent

scholarly journals Cell Metabolism Control Through O-GlcNAcylation of STAT5: A Full or Empty Fuel Tank Makes a Big Difference for Cancer Cell Growth and Survival

2019 ◽  
Vol 20 (5) ◽  
pp. 1028 ◽  
Author(s):  
Manuel Rauth ◽  
Patricia Freund ◽  
Anna Orlova ◽  
Stefan Grünert ◽  
Nikola Tasic ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tyrosine Phosphorylation ◽  
Cancer Cell ◽  
Metabolic Status ◽  
Dependent Manner ◽  
Post Translational Modification ◽  
Cancer Cell Growth ◽  
Hexosamine Biosynthetic Pathway ◽  
Growth And Survival ◽  
Cell Growth And Survival

O-GlcNAcylation is a post-translational modification that influences tyrosine phosphorylation in healthy and malignant cells. O-GlcNAc is a product of the hexosamine biosynthetic pathway, a side pathway of glucose metabolism. It is essential for cell survival and proper gene regulation, mirroring the metabolic status of a cell. STAT3 and STAT5 proteins are essential transcription factors that can act in a mutational context-dependent manner as oncogenes or tumor suppressors. They regulate gene expression for vital processes such as cell differentiation, survival, or growth, and are also critically involved in metabolic control. The role of STAT3/5 proteins in metabolic processes is partly independent of their transcriptional regulatory role, but is still poorly understood. Interestingly, STAT3 and STAT5 are modified by O-GlcNAc in response to the metabolic status of the cell. Here, we discuss and summarize evidence of O-GlcNAcylation-regulating STAT function, focusing in particular on hyperactive STAT5A transplant studies in the hematopoietic system. We emphasize that a single O-GlcNAc modification is essential to promote development of neoplastic cell growth through enhancing STAT5A tyrosine phosphorylation. Inhibition of O-GlcNAcylation of STAT5A on threonine 92 lowers tyrosine phosphorylation of oncogenic STAT5A and ablates malignant transformation. We conclude on strategies for new therapeutic options to block O-GlcNAcylation in combination with tyrosine kinase inhibitors to target neoplastic cancer cell growth and survival.

scholarly journals Cytotoxicity of Selenium Immunoconjugates against Triple Negative Breast Cancer Cells

2018 ◽  
Vol 19 (11) ◽  
pp. 3352 ◽  
Author(s):  
Soni Khandelwal ◽  
Mallory Boylan ◽  
Julian Spallholz ◽  
Lauren Gollahon
Keyword(s):  
Breast Cancer ◽  
Side Effects ◽  
Cell Growth ◽  
Cell Lines ◽  
Cancer Cell ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Dependent Manner ◽  
Breast Cancers ◽  
Cancer Cell Growth

Within the subtypes of breast cancer, those identified as triple negative for expression of estrogen receptor α (ESR1), progesterone receptor (PR) and human epidermal growth factor 2 (HER2), account for 10–20% of breast cancers, yet result in 30% of global breast cancer-associated deaths. Thus, it is critical to develop more targeted and efficacious therapies that also demonstrate less side effects. Selenium, an essential dietary supplement, is incorporated as selenocysteine (Sec) in vivo into human selenoproteins, some of which exist as anti-oxidant enzymes and are of importance to human health. Studies have also shown that selenium compounds hinder cancer cell growth and induce apoptosis in cancer cell culture models. The focus of this study was to investigate whether selenium-antibody conjugates could be effective against triple negative breast cancer cell lines using clinically relevant, antibody therapies targeted for high expressing breast cancers and whether selenium cytotoxicity was attenuated in normal breast epithelial cells. To that end, the humanized monoclonal IgG1 antibodies, Bevacizumab and Trastuzumab were conjugated with redox selenium to form Selenobevacizumab and Selenotrastuzumab and tested against the triple negative breast cancer (TNBC) cell lines MDA-MB-468 and MDA-MB-231 as well as a normal, immortalized, human mammary epithelial cell line, HME50-5E. VEGF and HER2 protein expression were assessed by Western. Although expression levels of HER2 were low or absent in all test cells, our results showed that Selenobevacizumab and Selenotrastuzumab produced superoxide (O2•−) anions in the presence of glutathione (GSH) and this was confirmed by a dihydroethidium (DHE) assay. Interestingly, superoxide was not elevated within HME50-5E cells assessed by DHE. The cytotoxicity of selenite and the selenium immunoconjugates towards triple negative cells compared to HME-50E cells was performed in a time and dose-dependent manner as measured by Trypan Blue exclusion, MTT assay and Annexin V assays. Selenobevacizumab and Selenotrastuzumab were shown to arrest the cancer cell growth but not the HME50-5E cells. These results suggest that selenium-induced toxicity may be effective in treating TNBC cells by exploiting different immunotherapeutic approaches potentially reducing the debilitating side effects associated with current TNBC anticancer drugs. Thus, clinically relevant, targeting antibody therapies may be repurposed for TNBC treatment by attachment of redox selenium.

TSPAN8 promotes colorectal cancer cell growth and migration in LSD1-dependent manner

Life Sciences ◽  
2020 ◽  
Vol 241 ◽  
pp. 117114 ◽  
Author(s):  
Hong-Sheng Zhang ◽  
Hui-Yun Liu ◽  
Zhen Zhou ◽  
Hong-Liang Sun ◽  
Min-Yao Liu
Keyword(s):  
Colorectal Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Colorectal Cancer Cell ◽  
Dependent Manner ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
And Migration

scholarly journals ZAK inhibits human lung cancer cell growth via ERK and JNK activation in an AP-1-dependent manner

2010 ◽  
Vol 101 (6) ◽  
pp. 1374-1381 ◽  
Author(s):  
Jaw-Ji Yang ◽  
Yi-Ju Lee ◽  
Hsin-Hung Hung ◽  
Wei-Pu Tseng ◽  
Chuan-Chou Tu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cell ◽  
Jnk Activation
Sign in / Sign up

Export Citation Format

Share Document