ArticleTranslational andrology and urology2019
Carcinoembryonic antigen related cell adhesion molecule 6 promotes the proliferation and migration of renal cancer cells through the ERK/AKT signaling pathway.
Article in Translational andrology and urology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 14 citations in OpenAlex.
- Profiling the pancreatic cancer secretome with metabolic glycoengineering.The Journal of biological chemistry · 2026Article
- Exploring the interactions of integrins and CEACAM6 (Review).Experimental and therapeutic medicine · 2025Review
- Chronic Exposure of Renal Progenitor Cells (HRTPT) to As (III) Implicates Microfibril Associated Protein 5 (MFAP5) in the Activation of Carcinoembryonic Antigen Related Cell Adhesion Molecules (CEACAM 5 and 6).Current issues in molecular biology · 2025Article
- Cytokine and epigenetic regulation of CEACAM6 mediates EGFR-driven signaling and drug response in lung adenocarcinoma.NPJ precision oncology · 2025Article
- The emerging roles of CEACAM6 in human cancer (Review).International journal of oncology · 2024Review
- CT109-SN-38, a Novel Antibody-drug Conjugate with Dual Specificity for CEACAM5 and 6, Elicits Potent Killing of Pancreatic Cancer Cells.Current cancer drug targets · 2024Article
- Identification of Early Events in Serrated Pathway Colorectal Tumorigenesis by Using Digital Spatial Profiling.Pathobiology : journal of immunopathology, molecular and cellular biology · 2024Article
- Evaluation of novel anti-CEACAM6 antibody-based conjugates for radioimmunotheranostics of pancreatic ductal adenocarcinoma.European radiology · 2023Article
- The m6A modification-mediated OGDHL exerts a tumor suppressor role in ccRCC by downregulating FASN to inhibit lipid synthesis and ERK signaling.Cell death & disease · 2023Article
- HOXB5-activated ANGPT2 promotes the proliferation, migration, invasion and angiogenic effect of esophageal cancer cells via activating ERK/AKT signaling pathway.Experimental and therapeutic medicine · 2022Article
- The role of long non-coding RNA FGD5-AS1 in cancer.Bioengineered · 2022Review
- Prognostic value of the immune target CEACAM6 in cancer: a meta-analysis.Therapeutic advances in medical oncology · 2022Article
- CEACAM6's Role as a Chemoresistance and Prognostic Biomarker for Pancreatic Cancer: A Comparison of CEACAM6's Diagnostic and Prognostic Capabilities with Those of CA19-9 and CEA.Life (Basel, Switzerland) · 2021Article
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCarcinoembryonic antigen related cell adhesion molecule 6 (CEACAM6) is a versatile glycoprotein and a member of the CEACAM family. Studies suggested that it served as a diagnostic and prognostic biomarker in some malignancies. In addition, it is involved in tumorigenesis by stimulating proliferation, suppressing apoptosis, facilitating migration and invasion, promoting angiogenesis, and inducing drug resistance. In the present study, we demonstrated the oncogenic effects of CEACAM6 in clear cell renal cell carcinoma (ccRCC).
methodsCEACAM6 expression was detected by quantitative real-time PCR (qRT-PCR), immunohistochemical staining and western blot in ccRCC tumor tissues and cell lines. Survival analysis was performed using the data of TCGA database. Cell proliferation and migration were detected by CCK-8 and transwell assays with the overexpression or silencing of CEACAM6. LY294002 was used to block the activation of PI3K/AKT pathway. Associated pathway proteins were detected by western blot.
resultsCEACAM6 was upregulated in ccRCC cell lines and tumor tissues. Longer overall survival was observed in patients with relatively low CEACAM6 levels. Furthermore, overexpression of CEACAM6 promoted the proliferation and migration of ccRCC cells. Conversely, shRNA-mediated CEACAM6 depletion modulated those changes. Further investigation demonstrated that the ERK/AKT signaling pathway activation played a pivotal role. In addition, PI3K/AKT pathway blockade abrogated the effects of CEACAM6 overexpression.
conclusionsAberrantly high expression of CEACAM6 is a stimulus for the formation and progression of ccRCC.
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