{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ye M"],"funding":["The Natural Science Foundation of Nantong","Nantong University","Lo Kwee Seong Start Up Fund","National Natural Science Foundation of China"],"pagination":["e13226"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9136492"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["55(5)"],"pubmed_abstract":["Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. However, the treatment regimens for TNBC are limited. Chromosome segregation 1-like (CSE1L), also called cellular apoptosis susceptibility protein (CAS), is highly expressed in breast cancer and plays a crucial role in the progression of various tumours. However, the involvement of CAS in TNBC remains elusive. In this study, we showed that the expression of CAS was higher in TNBC samples than in non-TNBC samples in the Gene Expression Omnibus database. Knockdown of CAS inhibited MDA-MB-231 cell growth, migration and invasion. Further RNA-seq analysis revealed that complement pathway activity was significantly elevated. Of note, complement component 3 (C3), the key molecule in the complement pathway, was s"],"journal":["Cell proliferation"],"pubmed_title":["Interfering with CSE1L/CAS inhibits tumour growth via C3 in triple-negative breast cancer."],"pmcid":["PMC9136492"],"funding_grant_id":["03083028, 03083011, 135419631032","81871202","JC2021081"],"pubmed_authors":["Ye M","Tian J","Liu J","Chen Y","Wang X","Chen H","Shi J","Fok KL"],"additional_accession":[]},"is_claimable":false,"name":"Interfering with CSE1L/CAS inhibits tumour growth via C3 in triple-negative breast cancer.","description":"Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. However, the treatment regimens for TNBC are limited. Chromosome segregation 1-like (CSE1L), also called cellular apoptosis susceptibility protein (CAS), is highly expressed in breast cancer and plays a crucial role in the progression of various tumours. However, the involvement of CAS in TNBC remains elusive. In this study, we showed that the expression of CAS was higher in TNBC samples than in non-TNBC samples in the Gene Expression Omnibus database. Knockdown of CAS inhibited MDA-MB-231 cell growth, migration and invasion. Further RNA-seq analysis revealed that complement pathway activity was significantly elevated. Of note, complement component 3 (C3), the key molecule in the complement pathway, was s","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2026-07-14T16:47:06.889Z","creation":"2025-04-07T09:44:39.856Z"},"accession":"S-EPMC9136492","cross_references":{"pubmed":["35403306"],"doi":["10.1111/cpr.13226"]}}