Alterations in APC, BECN1, and TP53 gene expression levels in colon cancer cells caused by monosodium glutamate

Abstract Colorectal cancer (CRC) is a disease with high incidence worldwide. As of 2018, it is the second leading cause of cancer deaths in the world. In Saudi Arabia, the incidence of this disease has been increasing in the younger population. Both genetic and lifestyle factors may have contributed to its increased incidence and pathogenesis. Monosodium glutamate (MSG) is a food flavor enhancer that can be found in many commercial foods, and it can sometimes be used as a substitute to table salt. MSG has been investigated for its possible genotoxicity, yielding controversial results. In the present study, the effect of MSG on cell viability and its effect on expression of APC, BECN1, and TP53 genes in SW620 and SW480 colon cancer cell lines were studied. TP53 is a tumor suppressor gene that functions in modifying DNA errors and/or inducing apoptosis of damaged cells, and both APC and BECN1 genes are involved in CRC and are of importance in cellular growth and metastasis. Cancer cell viability was analyzed using MTT assay, and the results showed a significant increase in the number of viable cells after 24 h of treatment with MSG with different concentrations (0.5, 1.0, 10, 50, and 100mM). Moreover, gene expression results showed a significant increase in the expression levels of APC and BECN1 under specified conditions in both cell lines; conversely, TP53 showed a significant decrease in expression in SW620 cells. Thus, it can be concluded that MSG possibly confers a pro-proliferative effect on CRC cells.

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Biological Effect of Organically Coated Grias neuberthii and Persea americana Silver Nanoparticles on HeLa and MCF-7 Cancer Cell Lines

Journal of Nanotechnology ◽

10.1155/2018/9689131 ◽

2018 ◽

Vol 2018 ◽

pp. 1-11 ◽

Cited By ~ 6

Author(s):

Lizeth Salazar ◽

María José Vallejo López ◽

Marcelo Grijalva ◽

Luis Castillo ◽

Alexander Maldonado

Keyword(s):

Gene Expression ◽

Transcription Factor ◽

Cell Viability ◽

Cell Lines ◽

Cancer Cell ◽

Hela Cells ◽

Biological Effect ◽

Persea Americana ◽

Expression Levels ◽

Mcf 7

The aim of this study was to assess the biological effect of organically coated Grias neuberthii (piton) fruit and Persea americana (avocado) leaves nanoparticles (NPs) on cervical cancer (HeLa) and breast adenocarcinoma (MCF-7) cells with an emphasis on gene expression (p53 transcription factor and glutathione-S-transferase GST) and cell viability. UV-Vis spectroscopy analysis showed that synthesized AgNPs remained partially stable under cell culture conditions. HeLa cells remained viable when exposed to piton and avocado AgNPs. A statistically significant, dose-dependent cytotoxic response to both AgNPs was found on the breast cancer (MCF-7) cell line at concentrations above 50 µM. While expression levels of transcription factor p53 showed downregulation in treated MCF-7 and HeLa cells, GST expression was not affected in both cell lines treated. Cell viability assays along with gene expression levels in treated MCF-7 cells support a cancer cell population undergoing cell cycle arrest. The selective toxicity of biosynthesized piton/avocado AgNPs on MCF-7 cells might be of value for novel therapeutics.

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Pharmaceutical immunoglobulin G impairs anti-carcinoma activity of oxaliplatin in colon cancer cells

British Journal of Cancer ◽

10.1038/s41416-021-01272-6 ◽

2021 ◽

Author(s):

Yuru Shang ◽

Xianbin Zhang ◽

Lili Lu ◽

Ke Jiang ◽

Mathias Krohn ◽

...

Keyword(s):

Colon Cancer ◽

Cell Viability ◽

Cancer Patients ◽

Cell Lines ◽

Cancer Cell ◽

Immunoglobulin G ◽

Cancer Cell Lines ◽

Human Igg ◽

Western Blots ◽

Igg Receptors

Abstract Background Recent evidence proves that intravenous human immunoglobulin G (IgG) can impair cancer cell viability. However, no study evaluated whether IgG application benefits cancer patients receiving chemotherapeutics. Methods Influence of pharmaceutical-grade human IgG on the viability of a series of patient-derived colon cancer cell lines with and without chemotherapeutic intervention was determined. Cell death was analysed flow cytometrically. In addition, the influence of oxaliplatin and IgG on the ERK1/2-signalling pathway was evaluated by western blots. Results We evaluated the effects of pharmaceutical IgG, such as PRIVIGEN® IgG and Tonglu® IgG, in combination with chemotherapeutics. We did not observe any significant effects of IgG on tumour cell viability directly; however, human IgG significantly impaired the anti-tumoral effects of oxaliplatin. Primary cancer cell lines express IgG receptors and accumulate human IgG intracellularly. Moreover, while oxaliplatin induced the activation of ERK1/2, the pharmaceutical IgG inhibited ERK1/2 activity. Conclusions The present study demonstrates that pharmaceutical IgG, such as PRIVIGEN® IgG and Tonglu® IgG, can impair the anti-carcinoma activity of oxaliplatin. These data strongly suggest that therapeutic IgG as co-medication might have harmful side effects in cancer patients. The clinical significance of these preclinical observations absolutely advises further preclinical, as well as epidemiological and clinical research.

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Development of myeloid-derived suppressor cells (MDSC) targeted therapy for the treatment of cisplatin-resistant bladder cancer.

Journal of Clinical Oncology ◽

10.1200/jco.2019.37.7_suppl.415 ◽

2019 ◽

Vol 37 (7_suppl) ◽

pp. 415-415

Author(s):

Yuji Takeyama ◽

Minoru Kato ◽

Yasuomi Shimizu ◽

Kosuke Hamada ◽

Taro Iguchi ◽

...

Keyword(s):

Gene Expression ◽

Bladder Cancer ◽

Cell Lines ◽

Cancer Cell ◽

Suppressor Cells ◽

Bladder Cancer Cell ◽

Myeloid Derived Suppressor Cells ◽

Expression Levels ◽

Tumor Bearing ◽

Gene Expression Levels

415 Background: The emergence of immune checkpoint inhibitors (ICI) has brought hope for cure and survival for those suffering from various cancers, including bladder cancer. However, the response rate of ICI monotherapy is modest, and recent reports indicate that myeloid-derived suppressor cells (MDSC) might play a role in the resistant mechanism of ICI. In this study, we assess the effect of chemokine signal on the proliferation of bladder cancer and investigate whether MDSC could be a new target for the treatment of cisplatin-resistant bladder cancer. Methods: We established a cisplatin resistant strain (MB49R) of mice bladder cancer cell line MB49, and examined the alteration of the expression levels of inflammatory chemokines by chemokine array. Next, we isolated MDSCs from spleen and tumor in tumor-bearing mice to examine gene expression levels of chemokine receptors (CXCR2 and CCR2) and immunosuppression genes (Arg-1 and iNOS). Furthermore, we assessed the efficacy of CDDP, α-PD-L1 and chemokine antagonists against the proliferation of tumors in MB49 and MB49R xenograft models. Results: Expression levels of CCL2 and CXCL1/2, which are involved in the migration of MDSC, were significantly increased in the culture supernatant of MB49R compared to those in MB49 cell lines. This result was confirmed by real-time RT-qPCR of tumor extract, and this increase was also observed in human bladder cancer cell lines (T24 and T24R). CXCR2 and CCR2 were highly expressed in PMN-MDSC and M-MDSC, respectively, which were isolated from spleen or tumors in tumor-bearing mice, and gene expression levels of Arg-1 and iNOS were dramatically increased in M-MDSCs from the tumor tissues compared to those from spleen. Also, analysis by flow cytometry revealed that PMN-MDSC dramatically decreased in MB49R compared to parental MB49 tumors, while the proportion of M-MDSC was not changed in MB49R, which indicates that M-MDSC could be a target for the treatment of CDDP resistant bladder cancer. Conclusions: The results in the present study might indicate that the combination treatment with ICI and MDSC-targeting therapy could be an option for the treatment of cisplatin-resistant bladder cancer.

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Gene Expression Profile of Colon Cancer Cell Lines Treated with SN38

2010 4th International Conference on Bioinformatics and Biomedical Engineering ◽

10.1109/icbbe.2010.5517918 ◽

2010 ◽

Author(s):

Ying Wang ◽

Jiajia Chen ◽

Bairong Shen ◽

Åsa Wallin ◽

Xiao-feng Sun

Keyword(s):

Gene Expression ◽

Colon Cancer ◽

Gene Expression Profile ◽

Cell Lines ◽

Cancer Cell ◽

Expression Profile ◽

Cancer Cell Lines ◽

Colon Cancer Cell ◽

Colon Cancer Cell Lines

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MicroRNA silencing of CNN1 and CNN2 protein family members regulates biology processes in colorectal cancer by targeting the p53 signal pathway

10.21203/rs.3.rs-38064/v1 ◽

2020 ◽

Author(s):

Fuda Huang ◽

Mingwei Wei ◽

Anmin Wang ◽

Ya Zhang ◽

Zebang Qin ◽

...

Keyword(s):

Colorectal Cancer ◽

Cell Cycle ◽

Colon Cancer ◽

Cell Lines ◽

Cancer Cell ◽

Cancer Cell Lines ◽

Colon Cancer Cell ◽

Expression Levels ◽

Colon Cancer Cell Lines ◽

Cancer Tissues

Abstract BackgroundCalponin was first defined as a striated muscle troponin T-like protein that binds actin thin filaments to regulate smooth muscle contraction. There are few studies of CNN1 and CNN2 in colorectal cancer, and the roles these two genes play in colorectal cancer cell lines and the mechanisms by which they act are unknown.MethodsWe used immunohistochemistry to identify expression of the two genes in the cancer tissues. RT-PCR was used to measure expression levels of microRNA. W performed western blots to measure changes in signaling pathways in the context of expression interference.Meanwhile, the same method was used to measure binding relationship between the two genes and key pathway proteins. To determine the relationship between microRNA and gene mRNA, we used the reporter gene method. We used the chi-square and t-test methods to analyze the significance and correlations of the data.Results and conclusionsExpression levels of CNN1 were lower in colon cancer tissues than in normal mucosal tissues. After downregulating CNN1, the cell cycle in colon cancer cell lines progressed quickly, and the expression of related pathway proteins also increased. Expression levels of CNN2 were higher in colon cancer tissues, and its downregulation significantly inhibited cell cycle progression in colon cancer cell lines. We confirmed correlations between the expression of microRNA and CNN2 using data analysis.Bars indicate ± standard errors.*p < 0.05; **p < 0.01 compared with the control. The inhibition of the expression of CNN2 mRNA using microRNA was confirmed using western blot. The combination of the two at the mechanism level was also demonstrated using the reporter gene method.

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Evaluation of retinoblastoma (Rb) and protein-53 (p53) gene expression levels in breast cancer cell lines (MCF-7) induced with some selected cytotoxic plants

Planta Medica ◽

10.1055/s-0033-1352052 ◽

2013 ◽

Vol 79 (13) ◽

Cited By ~ 1

Author(s):

TA Samuel ◽

B James ◽

T Oshodi ◽

U Odii ◽

OA Odukoya ◽

...

Keyword(s):

Breast Cancer ◽

Gene Expression ◽

Cell Lines ◽

Cancer Cell ◽

Breast Cancer Cell ◽

P53 Gene ◽

Breast Cancer Cell Lines ◽

Expression Levels ◽

Gene Expression Levels ◽

Mcf 7

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SRCgene expression in human cancer: the role of transcriptional activation

Biochemistry and Cell Biology ◽

10.1139/o03-077 ◽

2004 ◽

Vol 82 (2) ◽

pp. 263-274 ◽

Cited By ~ 107

Author(s):

Scott M Dehm ◽

Keith Bonham

Keyword(s):

Gene Expression ◽

Colon Cancer ◽

Tyrosine Kinase ◽

Cell Lines ◽

Cancer Cell ◽

Cellular Proliferation ◽

Human Cancer ◽

Cancer Cell Lines ◽

Src Gene ◽

Src Activation

Human pp60c-Src(or c-Src) is a 60 kDa nonreceptor tyrosine kinase encoded by the SRC gene and is the cellular homologue to the potent transforming v-Src viral oncogene. c-Src functions at the hub of a vast array of signal transduction cascades that influence cellular proliferation, differentiation, motility, and survival. c-Src activation has been documented in upwards of 50% of tumors derived from the colon, liver, lung, breast, and pancreas. Therefore, a major focus has been to understand the mechanisms of c-Src activation in human cancer. Early studies concentrated on post-translational mechanisms that lead to increased c-Src kinase activity, which often correlated with overexpression of c-Src protein. More recently, the discovery of an activating SRC mutation in a small subset of advanced colon tumors has been reported. In addition, elevated SRC transcription has been identified as yet another mechanism contributing significantly to c-Src activation in a subset of human colon cancer cell lines. Interestingly, histone deacetylase (HDAC) inhibitors, agents with well-documented anti-cancer activity, repress SRC transcription in a wide variety of human cancer cell lines. Analysis of the mechanisms behind HDAC inhibitor mediated repression could be utilized in the future to specifically inhibit SRC gene expression in human cancer.Key words: c-Src, tyrosine kinase, gene expression, transcription, colon cancer.

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