The role of C1orf50 in breast cancer progression and prognosis

被引:0
作者
Otani, Yusuke [1 ,2 ]
Tanaka, Atsushi [1 ,2 ]
Maekawa, Masaki [1 ,2 ]
Pena, Tirso [1 ,2 ]
Rogachevskaya, Anna [1 ,2 ]
Ando, Teruhiko [3 ]
Itano, Takuto [3 ]
Katayama, Haruyoshi [3 ]
Nakata, Eiji [3 ]
Ozaki, Toshifumi [3 ]
Toyooka, Shinichi [4 ]
Doihara, Hiroyoshi [5 ]
Roehrl, Michael H. [1 ,2 ]
Fujimura, Atsushi [6 ,7 ]
机构
[1] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA USA
[2] Harvard Med Sch, Boston, MA USA
[3] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Orthoped Surg, 2-5-1 Shikata Cho,Kita Ku, Okayama 7008558, Japan
[4] Okayama Univ, Dept Gen Thorac Surg & Breast & Endocrinol Surg, Grad Sch Med Dent & Pharmaceut Sci, 2-5-1 Shikata Cho,Kita Ku, Okayama 7008558, Japan
[5] Kawasaki Med Sch, Dept Gen Surg, Gen Med Ctr, 2-6-1 Nakasange,Kita Ku, Okayama 7008505, Japan
[6] Okayama Univ, Dept Cellular Physiol, Grad Sch Med Dent & Pharmaceut Sci, 2-5-1 Shikata Cho,Kita Ku, Okayama 7008558, Japan
[7] Okayama Univ, Neutron Therapy Res Ctr, 2-5-1 Shikata Cho,Kita Ku, Okayama 7008558, Japan
关键词
C1orf50; Luminal A breast cancer; Cell cycle; Immune evasion; YAP/TAZ; MOLECULAR SUBTYPES; EXPRESSION;
D O I
10.1007/s12282-024-01653-8
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Although the prognosis of breast cancer has significantly improved compared to other types of cancer, there are still some patients who expire due to recurrence or metastasis. Therefore, it is necessary to develop a method to identify patients with poor prognosis at the early stages of cancer. In the process of discovering new prognostic markers from genes of unknown function, we found that the expression of C1orf50 determines the prognosis of breast cancer patients, especially for those with Luminal A breast cancer. This study aims to elucidate the molecular role of C1orf50 in breast cancer progression. Bioinformatic analyses of the breast cancer dataset of TCGA, and in vitro analyses, reveal the molecular pathways influenced by C1orf50 expression. C1orf50 knockdown suppressed the cell cycle of breast cancer cells and weakened their ability to maintain the undifferentiated state and self-renewal capacity. Interestingly, upregulation of C1orf50 increased sensitivity to CDK4/6 inhibition. In addition, C1orf50 was found to be more abundant in breast cancer cells than in normal breast epithelium, suggesting C1orf50's involvement in breast cancer pathogenesis. Furthermore, the mRNA expression level of C1orf50 was positively correlated with the expression of PD-L1 and its related factors. These results suggest that C1orf50 promotes breast cancer progression through cell cycle upregulation, maintenance of cancer stemness, and immune evasion mechanisms. Our study uncovers the biological functions of C1orf50 in Luminal breast cancer progression, a finding not previously reported in any type of cancer.
引用
收藏
页码:292 / 305
页数:14
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