Carcinoembryonic antigen (CEACAM) family members and Inflammatory Bowel Disease

Kelleher, Maebh; Singh, Raminder; O’Driscoll, Caitriona M.; Melgar, Silvia

doi:10.1016/j.cytogfr.2019.05.008

Cited by 40 publications

(48 citation statements)

References 104 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Treatment with limonin reverted back the levels of these serum marker enzymes to near to normal, which is suggestive of its anticancer potential. CEA is a tumor‐related glycoprotein and one of the oncofetal antigens that have been broadly considered for its prospective function as a predictive indicator . An augmented level of the CEA in cancer‐bearing animals may relate to the production of tumor, stage, its location, size, vascularity, and differentiation .…”

Section: Discussionmentioning

confidence: 99%

“…CEA is a tumor-related glycoprotein and one of the oncofetal antigens that have been broadly considered for its prospective function as a predictive indicator. [38] An augmented level of the CEA in cancer-bearing animals may relate to the production of tumor, stage, its location, size, vascularity, and differentiation. [39] In the current study, an increased level of CEA was found in cancer-bearing mice and the same results were reported in a previous study.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Anticancer effect of Limonin against benzo(a)pyrene‐induced lung carcinogenesis in Swiss albino mice and the inhibition of A549 cell proliferation through apoptotic pathway

Gong

Huo

et al. 2019

J Biochem & Molecular Tox

View full text Add to dashboard Cite

The main purpose of the current study is to reveal the anticancer action of limonin against benzo(a)pyrene [B(a)P]‐treated lung carcinogenesis in Swiss albino mice and A549 lung cancer cells. B(a)P was orally supplemented (50 mg/kg body weight) twice a week for four weeks induction of lung cancer in mice. The lung weight, body weight, incidence of tumor, lipid peroxidation, carcinoembryonic antigen (CEA), enzymatic and nonenzymatic antioxidants (superoxide dismutase, GPx, glutathione, glutathione reductase, catalase, and glutathione S‐transferase), serum marker enzymes (aryl hydroxylase, lactate dehydrogenase, 5′‐nucleotidases, and γ‐glutamyl transpeptidase), and inflammatory mediators (interleukin‐1β, interleukin‐6, and tumor necrosis factor‐α) were estimated. Moreover, a histopathological study of lung tissues was supported by the biochemical analysis. Furthermore, the anticancer activity of limonin on A549 cells was measured by cell viability, production of reactive oxygen species (ROS), apoptotic morphological changes by AO/EtBr staining. Additionally, the status of apoptosis protein (caspase‐9 and ‐3) expressions was analyzed by the colorimetric analysis. B(a)P‐induced mice showed increased lipid peroxidation, CEA, serum marker enzymes and inflammatory cytokines levels with simultaneously decreased in the nonenzymatic and enzymatic antioxidants levels. Limonin supplements significantly reverted back to all these changes in this manner, showing the efficiency of anticancer effect. Furthermore, our in vitro study also supported the anticancer effect of the treatment of limonin‐enhanced apoptosis by loss of cell viability, improved ROS production, apoptotic morphological changes, and apoptosis protein expression were analyzed. Overall, these results suggest the anticancer potential of limonin against B(a)P‐induced lung cancer in Swiss albino mice and A549 lung cancer cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Anticancer effect of Limonin against benzo(a)pyrene‐induced lung carcinogenesis in Swiss albino mice and the inhibition of A549 cell proliferation through apoptotic pathway

Gong

Huo

et al. 2019

J Biochem & Molecular Tox

View full text Add to dashboard Cite

show abstract

“…These differentially used splice sites come from 246 genes, of which only 104 were found to be differentially expressed at the gene level, further supporting the suggestion of a “spliceopathy”. A representative example, CEACAM1, itself an established IBD risk gene [ 26 ] whose product regulates mucosal inflammation via T-cells [ 27 ], is shown in Fig. 2 b where exon bin 12 has low, rectal-like PSI in the ileum, whereas the other intermediate samples are more ileal-like.…”

Section: Resultsmentioning

confidence: 99%

Altered splicing associated with the pathology of inflammatory bowel disease

et al. 2021

View full text Add to dashboard Cite

Background Aberrant splicing of individual genes is a well-known mechanism promoting pathology for a wide range of conditions, but disease is less commonly attributed to global disruption of exon usage. To explore the possible association of aberrant splicing with inflammatory bowel disease, we developed a pipeline for quantifying transcript abundance and exon inclusion transcriptome-wide and applied it to a dataset of ileal and rectal biopsies, both obtained in duplicate from 34 pediatric or young adult cases of ulcerative colitis and Crohn’s disease. Results Expression and splicing covary to some extent, and eight individuals exhibited aberrant profiles that can be explained by altered ratios of epithelial to stromal and immune cells. Ancestry-related biases in alternative splicing accounting for 5% of the variance were also observed, in part also related to cell-type proportions. In addition, two individuals were identified who had 284 exons with significantly divergent percent spliced in exons, including in the established IBD risk gene CEACAM1, which caused their ileal samples to resemble the rectum. Conclusions These results imply that quantitative differences in splice usage contribute to the pathology of inflammatory bowel disease in a previously unrecognized manner.

show abstract

“…Although new tumor markers have emerged in recent years (15), no specific markers for GBC have been validated to improve diagnostic rates and targeted therapy. CEACAM proteins have been reported to play a role in cell adhesion, intercellular signaling, inflammation (16,17), tumor invasion, metastasis and apoptosis (18,19). CEACAM6 is a member of the family of CEACAMs, and is upregulated in solid tumors, especially digestive system tumors (20), with an important role in the tumorigenesis and development of digestive system tumors.…”

Section: Discussionmentioning

confidence: 99%

Effect of CEACAM6 silencing on the biological behavior of human gallbladder cancer cells

Tian

Zhang

2020

Oncol Lett

View full text Add to dashboard Cite

Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is abnormally expressed in various malignant tumors and thus represents a potential biomarker, although information regarding its role in gallbladder cancer (GBC) is limited. This study aimed to evaluate the expression of CEACAM6 in GBC and the effect of CEACAM6 gene silencing on the proliferation, migration, invasion and apoptosis of human GBC cells. Immunochemistry was used to evaluate CEACAM6 expression in 95 GBC specimens and 40 peritumoral tissue specimens. GBC-SD and SGC-996 cell lines were used for in vitro experiments. CEACAM6 was knocked down by transfection of targeted small interfering RNA (siRNA), and reverse-transcription quantitative PCR and western blot analysis were used to detect knockdown efficiency. Cell Counting Kit-8 and colony formation assays were undertaken to evaluate cell proliferation. Variations in cell migration and invasion were detected by wound-healing and Transwell assays, respectively. Flow cytometry was applied to measure cell apoptosis and cell cycle distribution. CEACAM6 gene expression was significantly greater in GBC tissues than in peritumoral tissues, and its positive expression was associated with poor prognosis. CEACAM6 mRNA and protein expression in the CEACAM6 siRNA treatment group was significantly lower than that in the negative control group and the blank group. CEACAM6 knockdown inhibited GBC cell proliferation, migration and invasion but promoted cell apoptosis. Western blot analysis of invasion-and apoptosis-related proteins matrix metalloproteinase-2, Vimentin, BCL-2 and BAX further confirmed CEACAM6 mRNA depletion promoted cell apoptosis and inhibited invasion. Additionally, CEACAM6 mRNA depletion affected the progression of the GBC cell cycle to increase cell distribution in G 0 /G 1 phase, and to reduce it in G 2 /M phase and S phase. These findings indicated that CEACAM6 overexpression may be related to the tumorigenesis and development of GBC. In summary, depletion of CEACAM6 mRNA suppressed the malignant biological behaviors of human gallbladder cancer cells.

show abstract

Carcinoembryonic antigen (CEACAM) family members and Inflammatory Bowel Disease

Cited by 40 publications

References 104 publications

Anticancer effect of Limonin against benzo(a)pyrene‐induced lung carcinogenesis in Swiss albino mice and the inhibition of A549 cell proliferation through apoptotic pathway

Anticancer effect of Limonin against benzo(a)pyrene‐induced lung carcinogenesis in Swiss albino mice and the inhibition of A549 cell proliferation through apoptotic pathway

Altered splicing associated with the pathology of inflammatory bowel disease

Effect of CEACAM6 silencing on the biological behavior of human gallbladder cancer cells

Contact Info

Product

Resources

About