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Total 665 results found since Jan 2013.

FAM83D knockdown regulates proliferation, migration and invasion of colorectal cancer through inhibiting FBXW7/Notch-1 signalling pathway.
In conclusion, FAM83D knockdown promoted colorectal cancer cell apoptosis, inhibited cell proliferation, cell migration and invasion, which might be associated with inhibiting the FBXW7/Notch1 signal pathway. Our findings indicated that FAM83D is a promising molecular target for colorectal cancer treatment. PMID: 28407575 [PubMed - as supplied by publisher]
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - April 10, 2017 Category: Drugs & Pharmacology Authors: Mu Y, Zou H, Chen B, Fan Y, Luo S Tags: Biomed Pharmacother Source Type: research

Snail transcription factor NLS and importin β1 regulate the subcellular localization of Cathepsin L and Cux1.
Abstract Several recent studies have highlighted an additional unexpected localization and site of action for Cathepsin L (Cat L) protease within the nucleus in breast, colon and prostate cancer, however, its role in the nucleus was unclear. It was proposed to mediate proteolytic processing of the transcription factor CCAAT-displacement protein/cut homeobox transcription factor (Cux1) from the full-length p200 isoform to generate the p110 and p90 isoforms, of which the p110 isoform was shown to act as a cell cycle regulator to accelerate entry into the S phase. The p110 isoform has also been shown to bind to the p...
Source: Biochemical and Biophysical Research communications - July 8, 2017 Category: Biochemistry Authors: Burton LJ, Henderson V, Liburd L, Odero-Marah VA Tags: Biochem Biophys Res Commun Source Type: research

Evaluation of antitumor activity of survivin short interfering RNA delivered by lipid nanoparticles in colon cancer in vitro and in vivo.
Authors: Wang T, Liu Z, Zhang Z, Tang S, Yue M, Feng S, Hu M, Xuan L, Chen Y Abstract Survivin has been overexpressed in numerous types of cancer and is associated with a poor clinical outcome. A number of various approaches have been used to counteract survivin in order to inhibit tumor growth or promote cell apoptosis. The present study aimed to evaluate the efficiency and antitumor effect of a survivin-targeted short interfering RNA (siRNA) delivery system using lipid nanoparticles for the treatment of colon cancer. Survivin siRNA (si-survivin) nanoliposomes were prepared and transfected into LoVo cells. The mRN...
Source: Oncology Letters - August 9, 2017 Category: Cancer & Oncology Tags: Oncol Lett Source Type: research

Abstract A25: Synthetic lethal CRISPR-Cas9 screen imply an oncogenic role for FBXW7 mutations in colon cancer
Mutations in tumour suppressors and un-druggable oncogenes dominate the landscape of cancer driver genes. Only a minority of colon cancers have mutations in druggable cancer drivers, such as PIK3CA. Conversely, mutations in tumour suppressors such as APC and TP53 are frequent, as are mutations in the notoriously difficult to drug KRAS target. There is an urgent need for new therapeutics to target tumours driven by these mutations: immune checkpoint approaches are likely to only prove effective in the fraction of patients whose tumours bear high mutation loads, which is colon cancer may be restricted to the minority of mism...
Source: Molecular Cancer Therapeutics - October 2, 2017 Category: Cancer & Oncology Authors: Moore, J. D., Hudson, C., Russell, P., Tiwana, G., Walter, D., Wiggins, C. M., Yarker, J. Tags: Finding Synthetic Lethal Interactions through Functional Genomics: Poster Presentations - Proffered Abstracts Source Type: research

Reduced Lipocalin 2 Expression Contributes to Vincristine Resistance in Human Colon Cancer Cellsance in Human Colon Cancer Cells.
CONCLUSION: Overall, these results demonstrate that LCN2 plays an important role in VCR resistance and is a potential therapeutic target for this disease. PMID: 29268690 [PubMed - as supplied by publisher]
Source: Recent Patents on Anti-Cancer Drug Discovery - December 23, 2017 Category: Cancer & Oncology Tags: Recent Pat Anticancer Drug Discov Source Type: research

MiRNA-155 promotes the invasion of colorectal cancer SW-480 cells through regulating the Wnt/ β-catenin.
CONCLUSIONS: The findings of this study suggest that miR-155 and β-catenin may have a unique potential as a novel biomarker candidate for diagnosis and treatment of tumor metastasis. PMID: 29364476 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - January 26, 2018 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Inhibition of autophagy enhances DENSpm-induced apoptosis in human colon cancer cells in a p53 independent manner
ConclusionsFrom our results we conclude that DENSpm-induced apoptotic cell death is increased when autophagy is inhibited by 3-MA or Beclin-1 siRNA through PA depletion and PA catabolic activation in colon cancer cells, regardless p53 mutation status.
Source: Cellular Oncology - February 28, 2018 Category: Cancer & Oncology Source Type: research

ROS Modifiers and NOX4 Affect the Expression of the Survivin-Associated Radio-Adaptive Response.
Abstract The survivin-associated radio-adaptive response can be induced following exposure to ionizing radiation in the dose range from 5 to 100 mGy, and its magnitude of expression is dependent upon the TP53 mutational status of cells and ROS signaling. The purpose of the study was to investigate the potential role of ROS in the development of the survivin-associated adaptive response. Utilizing human colon carcinoma HCT116 TP53 wild type (WT) and HCT116 isogenic TP53 null mutant (Mut) cell cultures, the roles of inter- and intracellular ROS signaling on expression of the adaptive response as evidenced by changes...
Source: Free Radical Biology and Medicine - April 13, 2018 Category: Biology Authors: Murley JS, Arbiser JL, Weichselbaum RR, Grdina DJ Tags: Free Radic Biol Med Source Type: research

Let ‑7d inhibits colorectal cancer cell proliferation through the CST1/p65 pathway.
Let‑7d inhibits colorectal cancer cell proliferation through the CST1/p65 pathway. Int J Oncol. 2018 May 23;: Authors: Jiang J, Liu HL, Tao L, Lin XY, Yang YD, Tan SW, Wu B Abstract Cystatin SN (cystatin 1, CST1) is a member of the cystatin superfamily which inhibits the proteolytic activity of cysteine proteases. CST1 is a tumor biomarker that provides useful information for the diagnosis of esophageal, gastric and colorectal carcinomas. MicroRNAs (miRNAs or miRs) play an important role in tumor cell proliferation. However, the exact role of let‑7d and CST1 in colon cancer remains unknown. The a...
Source: International Journal of Oncology - May 23, 2018 Category: Cancer & Oncology Authors: Jiang J, Liu HL, Tao L, Lin XY, Yang YD, Tan SW, Wu B Tags: Int J Oncol Source Type: research

Upregulation of RASSF1A in Colon Cancer by Suppression of Angiogenesis Signaling and Akt Activation
Conclusion: Our results demonstrate for the first time that AGP induces RASSF1A expression in colon cancer cells and is dependent on angiogenesis signaling events. Therefore, our research may facilitate novel therapeutic options for advanced colon cancer therapy.Cell Physiol Biochem 2018;48:1259 –1273
Source: Cellular Physiology and Biochemistry - July 25, 2018 Category: Cytology Source Type: research

The JAK/STAT Pathway in Skeletal Muscle Pathophysiology
Conclusion and Perspectives The IL-6/JAK/STAT signaling cascade plays a dominant role in skeletal muscle pathophysiology. IL-6 autocrine, paracrine, and endocrine functions assign to its downstream effectors pivotal importance in skeletal muscle-wasting-associated diseases and other multiple system diseases where muscle acts in communication with other organs. Targeting the components of the JAK/STAT pathway recently emerged as a strategic approach for the treatment of inflammatory diseases and human cancer. This review highlights the opposite outcomes on muscle biology caused by the amount of local and systemic release ...
Source: Frontiers in Physiology - April 29, 2019 Category: Physiology Source Type: research

Induction of Trop-2 expression through the binding of galectin-3 to MUC1.
Abstract Both mucin 1 (MUC1) and trophoblast cell surface antigen 2 (Trop-2) are overexpressed in various epithelial tumor cells, and their high expression is correlated with a poor prognosis. Both proteins were expressed in a human breast cancer cell line, MCF-7 cells, but neither was in a human colon cancer cell line, HCT116 cells. When MUC1 cDNA was introduced into HCT116 cells (HCT116/MUC1), expression of Trop-2 was induced. Reciprocally, treatment of MCF-7 cells with MUC1 siRNA reduced the level of Trop-2. Mithramycin A, an inhibitor of specificity protein 1 (Sp1) transcription factor, effectively inh...
Source: Biochemical and Biophysical Research communications - June 9, 2019 Category: Biochemistry Authors: Yamashita T, Mori Y, Alzaaqi SM, Yashiro M, Sawada T, Hirakawa K, Nakada H Tags: Biochem Biophys Res Commun Source Type: research

lncRNA CCAT1 promotes bladder cancer cell proliferation, migration and invasion
Conclusion: CCAT1 plays an oncogenic role in urothelial carcinoma of the bladder. In addition, CCAT1 may be a potential therapeutic target in this cancer.
Source: International Braz J Urol - June 27, 2019 Category: Urology & Nephrology Source Type: research

Long non-coding RNA CCAT1 is overexpressed in endometrial cancer and regulates growth and transcriptome of endometrial adenocarcinoma cells.
CONCLUSIONS: Given that the lncRNA CCAT1 was found to be overexpressed in endometrial cancer, affected the growth of HEC-1B cells and the expression of growth regulatory genes, our data suggest CCAT1 to exert oncogenic functions in endometrial cancer and encourage further studies to examine to what extent this lncRNA might be a potential therapy target in this cancer entity. PMID: 32173521 [PubMed - as supplied by publisher]
Source: The International Journal of Biochemistry and Cell Biology - March 11, 2020 Category: Biochemistry Authors: Treeck O, Skrzypczak M, Schüler-Toprak S, Weber F, Ortmann O Tags: Int J Biochem Cell Biol Source Type: research

Syndecan-1-Dependent Regulation of Heparanase Affects Invasiveness, Stem Cell Properties, and Therapeutic Resistance of Caco2 Colon Cancer Cells
The heparan sulfate proteoglycan Syndecan-1 binds cytokines, morphogens and extracellular matrix components, regulating cancer stem cell properties and invasiveness. Syndecan-1 is modulated by the heparan sulfate-degrading enzyme heparanase, but the underlying regulatory mechanisms are only poorly understood. In colon cancer pathogenesis, complex changes occur in the expression pattern of Syndecan-1 and heparanase during progression from well-differentiated to undifferentiated tumors. Loss of Syndecan-1 and increased expression of heparanase are associated with a change in phenotypic plasticity and an increase in invasiven...
Source: Frontiers in Oncology - May 13, 2020 Category: Cancer & Oncology Source Type: research