scholarly journals The impact of RNA binding motif protein 4-regulated splicing cascade on the progression and metabolism of colorectal cancer cells

Oncotarget ◽  
2015 ◽  
Vol 6 (35) ◽  
pp. 38046-38060 ◽  
Author(s):  
Yu-Chih Liang ◽  
Wei-Cheng Lin ◽  
Ying-Ju Lin ◽  
Jung-Chun Lin
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Rna Binding ◽  
Binding Motif ◽  
Colorectal Cancer Cells ◽  
The Impact

scholarly journals Cortisol and Testosterone Induce Bax and Bcl-2 Gene Expression and Caspases-8 and -9 Activity in Colon Cancer Cells (ht29) and Reduced the Cell Viability

2021 ◽  
Author(s):  
Amin Sarkhosh ◽  
Rahim Ahmadi ◽  
Seyyed Hossein Khatami ◽  
Hadi Ghasemi
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Colorimetric Method ◽  
Caspase 8 ◽  
Activity Levels ◽  
Colon Cancer Cells ◽  
Expression Levels ◽  
Colorectal Cancer Cells ◽  
The Impact

Abstract Cortisol and testosterone can inhibit the proliferation of colorectal cancer cells. Cortisol may augment the anti-cancer activity of testosterone in colorectal cancer cells. This research aimed to assess the impact of cortisol and testosterone on the viability of colon cancer cells (HTCs). The cytotoxic effects of cortisol and testosterone were evaluated using the MTT assay. Bax and Bcl-2 expression levels were determined using real-time PCR. The colorimetric method was used to assess the activity of caspase-8 and -9 enzymes. The expression levels of Bax and Bcl-2 genes significantly increased (p<0.001), as well as the activity levels of caspase-8 and -9, were elevated (p<0.001). Testosterone may exert cytotoxic activity in colon cancer cells in the presence of cortisol, and cortisol and testosterone cotreatment may contribute to the elevated Bax and Bcl-2 genes expression and caspase 8 and 9 activity enhancement in colorectal cancer cells.

scholarly journals The Impact of Molecular Hydrogen on Mitochondrial ROS and Apoptosis in Colorectal Cancer Cells

2021 ◽  
Vol 120 (3) ◽  
pp. 349a
Author(s):  
Yi-Hsuan Tsai ◽  
Megha Jhunjhunwala ◽  
Tsan-Yao Chen ◽  
Chi-Shuo Chen
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Molecular Hydrogen ◽  
Mitochondrial Ros ◽  
Colorectal Cancer Cells ◽  
The Impact

scholarly journals The Roles of Carcinoembryonic Antigen in Liver Metastasis and Therapeutic Approaches

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Joo Han Lee ◽  
Seong-Wook Lee
Keyword(s):  
Colorectal Cancer ◽  
Liver Metastasis ◽  
Carcinoembryonic Antigen ◽  
Cancer Cells ◽  
Rna Binding ◽  
Close Correlation ◽  
Cell Receptor ◽  
Receptor Protein ◽  
Cancer Cell Death ◽  
Colorectal Cancer Cells

Metastasis is a highly complicated and sequential process in which primary cancer spreads to secondary organic sites. Liver is a well-known metastatic organ from colorectal cancer. Carcinoembryonic antigen (CEA) is expressed in most gastrointestinal, breast, and lung cancer cells. Overexpression of CEA is closely associated with liver metastasis, which is the main cause of death from colorectal cancer. CEA is widely used as a diagnostic and prognostic tumor marker in cancer patients. It affects many steps of liver metastasis from colorectal cancer cells. CEA inhibits circulating cancer cell death. CEA also binds to heterogeneous nuclear RNA binding protein M4 (hnRNP M4), a Kupffer cell receptor protein, and activates Kupffer cells to secrete various cytokines that change the microenvironments for the survival of colorectal cancer cells in the liver. CEA also activates cell adhesion-related molecules. The close correlation between CEA and cancer has spurred the exploration of many CEA-targeted approaches as anticancer therapeutics. Understanding the detailed functions and mechanisms of CEA in liver metastasis will provide great opportunities for the improvement of anticancer approaches against colorectal cancers. In this report, the roles of CEA in liver metastasis and CEA-targeting anticancer modalities are reviewed.

scholarly journals The impact of the RBM4-initiated splicing cascade on modulating the carcinogenic signature of colorectal cancer cells

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Jung-Chun Lin ◽  
Yuan-Chii Lee ◽  
Yu-Chih Liang ◽  
Yang C. Fann ◽  
Kory R. Johnson ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Colorectal Cancer Cells ◽  
The Impact

scholarly journals Butyrate Suppresses Glucose Metabolism of Colorectal Cancer Cells via GPR109a-AKT Signaling Pathway and Enhances Chemotherapy

2021 ◽  
Vol 8 ◽  
Author(s):  
Hong-Wei Geng ◽  
Feng-Yi Yin ◽  
Zhi-Fa Zhang ◽  
Xu Gong ◽  
Yun Yang
Keyword(s):  
Colorectal Cancer ◽  
Glucose Metabolism ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Histone Deacetylases ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Anti Cancer ◽  
Colorectal Cancer Cells ◽  
The Impact

Glycolysis inhibitors are promising therapeutic drugs for tumor treatment, which target the uniquely elevated glucose metabolism of cancer cells. Butyrate is a critical product of beneficial microbes in the colon, which exerts extraordinary anti-cancer activities. In particular, butyrate shows biased inhibitory effects on the cell growth of cancerous colonocytes, whereas it is the major energy source for normal colonocytes. Besides its roles as the histone deacetylases (HDACs) inhibitor and the ligand for G-protein coupled receptor (GPR) 109a, the influence of butyrate on the glucose metabolism of cancerous colonocytes and the underlying molecular mechanism are not fully understood. Here, we show that butyrate markedly inhibited glucose transport and glycolysis of colorectal cancer cells, through reducing the abundance of membrane GLUT1 and cytoplasmic G6PD, which was regulated by the GPR109a-AKT signaling pathway. Moreover, butyrate significantly promoted the chemotherapeutical efficacy of 5-fluorouracil (5-FU) on cancerous colonocytes, with exacerbated impairment of DNA synthesis efficiency. Our findings provide useful information to better understand the molecular basis for the impact of butyrate on the glucose metabolism of colorectal cancer cells, which would promote the development of beneficial metabolites of gut microbiota as therapeutical or adjuvant anti-cancer drugs.

scholarly journals Targeting the tumor metabolism by oxamate potentiates the impact of chemotherapeutics in colorectal cancer cells

2021 ◽  
Author(s):  
Gizem ÇALIBAŞI KOÇAL ◽  
Çağrı ÇAKICI ◽  
Feriha TOKSÖZ ◽  
Şeniz İNANÇ SÜRER ◽  
Tolga SEVER ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Tumor Metabolism ◽  
Colorectal Cancer Cells ◽  
The Impact

scholarly journals IMCA Induces Ferroptosis Mediated by SLC7A11 through the AMPK/mTOR Pathway in Colorectal Cancer

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Lei Zhang ◽  
Wen Liu ◽  
Fangyan Liu ◽  
Qun Wang ◽  
Mengjiao Song ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Screening Tests ◽  
Therapeutic Drug ◽  
Solute Carrier Family ◽  
Colorectal Cancer Cells ◽  
Solute Carrier ◽  
The Impact

Ferroptosis, implicated in several diseases, is a new form of programmed and nonapoptotic cell death triggered by iron-dependent lipid peroxidation after inactivation of the cystine/glutamate antiporter system xc–, which is composed of solute carrier family 7 membrane 11 (SLC7A11) and solute carrier family 3 membrane 2 (SLC3A2). Therefore, inducing ferroptosis through inhibiting the cystine/glutamate antiporter system xc– may be an effective way to treat cancer. In previous screening tests, we found that the benzopyran derivative 2-imino-6-methoxy-2H-chromene-3-carbothioamide (IMCA) significantly inhibited the viability of colorectal cancer cells. However, the impact of IMCA on ferroptosis remains unknown. Hence, this study investigated the effect of IMCA on ferroptosis and elucidated the underlying molecular mechanism. Results showed that IMCA significantly inhibited the cell viability of colorectal cancer cells in vitro and inhibited tumor growth with negligible organ toxicity in vivo. Further studies showed that IMCA significantly induced the ferroptosis of colorectal cancer cells. Mechanistically, IMCA downregulated the expression of SLC7A11 and decreased the contents of cysteine and glutathione, which resulted in reactive oxygen species accumulation and ferroptosis. Furthermore, overexpression of SLC7A11 significantly attenuated the ferroptosis caused by IMCA. In addition, IMCA regulated the activity of the AMPK/mTOR/p70S6k signaling pathway, which is related to the activity of SLC7A11 and ferroptosis. Collectively, our research provided experimental evidences on the activity and mechanism of ferroptosis induced by IMCA and revealed that IMCA might be a promising therapeutic drug for colorectal cancer.

scholarly journals Inhibition of Liver Metastasis in Colorectal Cancer by Targeting IL-13/IL13Rα2 Binding Site with Specific Monoclonal Antibodies

Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1731
Author(s):  
Marta Jaén ◽  
Rubén A. Bartolomé ◽  
Carmen Aizpurua ◽  
Ángela Martin-Regalado ◽  
J. Ignacio Imbaud ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Monoclonal Antibodies ◽  
Liver Metastasis ◽  
Cancer Cells ◽  
Metastatic Cancer ◽  
Receptor Internalization ◽  
Binding Motif ◽  
Pathway Activation ◽  
Colorectal Cancer Cells

Background: IL13Rα2 is reportedly a promising therapeutic target in different cancers. Still, no specific antagonists have reached the clinics yet. We investigated the use of a IL-13/IL13Rα2 binding motif, called D1, as a new target for the development of therapeutic monoclonal antibodies (mAbs) for colorectal cancer (CRC) metastasis. Methods: IL13Rα2 D1 peptides were prepared and used for immunization and antibody development. Antibodies were tested for inhibition of cellular invasion through Matrigel using CRC cell lines. Effects of the mAbs on cell signaling, receptor internalization and degradation were determined by western blot and flow cytometry. Swiss nude mice were used for survival analysis after treatment with IL13Rα2-specific mAbs and metastasis development. Results: IL13Rα2 D1 peptides were used to generate highly selective mAbs that blocked IL13/IL13Rα2-mediated SRC activation and cell invasion in colorectal cancer cells. Antibodies also provoked a significant reduction in cell adhesion and proliferation of metastatic cancer cells. Treatment with mAbs impaired the FAK, SRC and PI3K/AKT pathway activation. Blocking effectivity was shown to correlate with the cellular IL13Rα2 expression level. Despite mAb 5.5.4 partially blocked IL-13 mediated receptor internalization from the cancer cell surface it still promotes receptor degradation. Compared with other IL13Rα2-specific antibodies, 5.5.4 exhibited a superior efficacy to inhibit metastatic growth in vivo, providing a complete mouse survival in different conditions, including established metastasis. Conclusions: Monoclonal antibody 5.5.4 showed a highly selective blocking capacity for the interaction between IL-13 and IL13Rα2 and caused a complete inhibition of liver metastasis in IL13Rα2-positive colorectal cancer cells. This capacity might be potentially applicable to other IL13Rα2-expressing tumors.

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