Erratum to:SCIENCE CHINA Life Sciences,Volume 66,Issue 12:2805-2817(2023),https://doi.org/10.1007/s11427-023-2343-y.This paper contains errors in Figure 1B and Figure 5A,where the representative images of immunohistoc...Erratum to:SCIENCE CHINA Life Sciences,Volume 66,Issue 12:2805-2817(2023),https://doi.org/10.1007/s11427-023-2343-y.This paper contains errors in Figure 1B and Figure 5A,where the representative images of immunohistochemical staining of FSIP1 in TNBC tissues and Western blot band of Nanog in 231-WT and 231-F KO cells were misused.展开更多
CDK4/6 inhibitors are routinely recommended agents for the treatment of advanced HR+HER2-breast cancer.However,their therapeutic effectiveness in triple-negative breast cancer(TNBC)remains controversial.Here,we observ...CDK4/6 inhibitors are routinely recommended agents for the treatment of advanced HR+HER2-breast cancer.However,their therapeutic effectiveness in triple-negative breast cancer(TNBC)remains controversial.Here,we observed that the expression level of fibrous sheath interacting protein 1(FSIP1)could predict the treatment response of TNBC to CDK4/6 inhibitors.High FSIP1 expression level was related to a poor prognosis in TNBC,which was associated with the ability of FSIP1 to promote tumor cell proliferation.FSIP1 downregulation led to slowed tumor growth and reduced lung metastasis in TNBC.FSIP1knockout caused cell cycle arrest at the G0/G1 phase and reduced treatment sensitivity to CDK4/6 inhibitors by inactivating the Nanog/CCND1/CDK4/6 pathway.FSIP1 could form a complex with Nanog,protecting it from ubiquitination and degradation,which may facilitate the rapid cell cycle transition from G0/G1 to S phase and exhibit enhanced sensitivity to CDK4/6 inhibitors.Our findings suggest that TNBC patients with high FSIP1 expression levels may be suitable candidates for CDK4/6 inhibitor treatment.展开更多
文摘Erratum to:SCIENCE CHINA Life Sciences,Volume 66,Issue 12:2805-2817(2023),https://doi.org/10.1007/s11427-023-2343-y.This paper contains errors in Figure 1B and Figure 5A,where the representative images of immunohistochemical staining of FSIP1 in TNBC tissues and Western blot band of Nanog in 231-WT and 231-F KO cells were misused.
基金supported by the National Natural Science Foundation of China (82203804,81872159)345 Talent Project of Shengjing Hospital of China Medical University。
文摘CDK4/6 inhibitors are routinely recommended agents for the treatment of advanced HR+HER2-breast cancer.However,their therapeutic effectiveness in triple-negative breast cancer(TNBC)remains controversial.Here,we observed that the expression level of fibrous sheath interacting protein 1(FSIP1)could predict the treatment response of TNBC to CDK4/6 inhibitors.High FSIP1 expression level was related to a poor prognosis in TNBC,which was associated with the ability of FSIP1 to promote tumor cell proliferation.FSIP1 downregulation led to slowed tumor growth and reduced lung metastasis in TNBC.FSIP1knockout caused cell cycle arrest at the G0/G1 phase and reduced treatment sensitivity to CDK4/6 inhibitors by inactivating the Nanog/CCND1/CDK4/6 pathway.FSIP1 could form a complex with Nanog,protecting it from ubiquitination and degradation,which may facilitate the rapid cell cycle transition from G0/G1 to S phase and exhibit enhanced sensitivity to CDK4/6 inhibitors.Our findings suggest that TNBC patients with high FSIP1 expression levels may be suitable candidates for CDK4/6 inhibitor treatment.
