TY - JOUR
T1 - LINC00355 regulates p27KIP expression by binding to MENIN to induce proliferation in late-stage relapse breast cancer
AU - Eteleeb, Abdallah M.
AU - Thunuguntla, Prasanth K.
AU - Gelev, Kyla Z.
AU - Tang, Cynthia Y.
AU - Rozycki, Emily B.
AU - Miller, Alexander
AU - Lei, Jonathan T.
AU - Jayasinghe, Reyka G.
AU - Dang, Ha X.
AU - White, Nicole M.
AU - Reis-Filho, Jorge S.
AU - Mardis, Elaine R.
AU - Ellis, Matthew J.
AU - Ding, Li
AU - Silva-Fisher, Jessica M.
AU - Maher, Christopher A.
N1 - Funding Information:
J.S.F. received funding from the Washington University School of Medicine Molecular Oncology Training Grant (T32CA113275) and Faculty Diversity Scholar Award. C.A.M. received funding from the Susan G. Komen Career Catalyst Award. M.J.E. received funding from a Susan G. Komen Promise Grant (PG12220321), a Cancer Prevention Institute of Texas (CPRIT) Recruitment of Established Investigators Award (RR140033), the AVON Foundation and the McNair Foundation, the Breast Cancer Research Foundation (BCRF ELFF-16-003), and R01-CA095614. J.S.R-F. is funded in part by the by a Cancer Center Support Grant of the National Institutes of Health (NIH)/ National Cancer Institute (grant No P30CA008748), by an NIH/NCI P50 CA247749 01 grant and by a Breast Cancer Research Foundation grant. We thank the Alvin J. Siteman Cancer Center at Washington University School of Medicine and Barnes-Jewish Hospital in St. Louis, MO., for the use of the Siteman Flow Cytometry that provided flow cytometry service. The GTEx Project was supported by the Common Fund of the Office of the Director of the National Institutes of Health, and by NCI, NHGRI, NHLBI, NIDA, NIMH, and NINDS.
Funding Information:
J.S.F. received funding from the Washington University School of Medicine Molecular Oncology Training Grant (T32CA113275) and Faculty Diversity Scholar Award. C.A.M. received funding from the Susan G. Komen Career Catalyst Award. M.J.E. received funding from a Susan G. Komen Promise Grant (PG12220321), a Cancer Prevention Institute of Texas (CPRIT) Recruitment of Established Investigators Award (RR140033), the AVON Foundation and the McNair Foundation, the Breast Cancer Research Foundation (BCRF ELFF-16-003), and R01-CA095614. J.S.R-F. is funded in part by the by a Cancer Center Support Grant of the National Institutes of Health (NIH)/ National Cancer Institute (grant No P30CA008748), by an NIH/NCI P50 CA247749 01 grant and by a Breast Cancer Research Foundation grant. We thank the Alvin J. Siteman Cancer Center at Washington University School of Medicine and Barnes-Jewish Hospital in St. Louis, MO., for the use of the Siteman Flow Cytometry that provided flow cytometry service. The GTEx Project was supported by the Common Fund of the Office of the Director of the National Institutes of Health, and by NCI, NHGRI, NHLBI, NIDA, NIMH, and NINDS.
Publisher Copyright:
© 2022, This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.
PY - 2022/12
Y1 - 2022/12
N2 - Late-stage relapse (LSR) in patients with breast cancer (BC) occurs more than five years and up to 10 years after initial treatment and has less than 30% 5-year relative survival rate. Long non-coding RNAs (lncRNAs) play important roles in BC yet have not been studied in LSR BC. Here, we identify 1127 lncRNAs differentially expressed in LSR BC via transcriptome sequencing and analysis of 72 early-stage and 24 LSR BC patient tumors. Decreasing expression of the most up-regulated lncRNA, LINC00355, in BC and MCF7 long-term estrogen deprived cell lines decreases cellular invasion and proliferation. Subsequent mechanistic studies show that LINC00355 binds to MENIN and changes occupancy at the CDKN1B promoter to decrease p27Kip. In summary, this is a key study discovering lncRNAs in LSR BC and LINC00355 association with epigenetic regulation and proliferation in BC.
AB - Late-stage relapse (LSR) in patients with breast cancer (BC) occurs more than five years and up to 10 years after initial treatment and has less than 30% 5-year relative survival rate. Long non-coding RNAs (lncRNAs) play important roles in BC yet have not been studied in LSR BC. Here, we identify 1127 lncRNAs differentially expressed in LSR BC via transcriptome sequencing and analysis of 72 early-stage and 24 LSR BC patient tumors. Decreasing expression of the most up-regulated lncRNA, LINC00355, in BC and MCF7 long-term estrogen deprived cell lines decreases cellular invasion and proliferation. Subsequent mechanistic studies show that LINC00355 binds to MENIN and changes occupancy at the CDKN1B promoter to decrease p27Kip. In summary, this is a key study discovering lncRNAs in LSR BC and LINC00355 association with epigenetic regulation and proliferation in BC.
UR - http://www.scopus.com/inward/record.url?scp=85128230136&partnerID=8YFLogxK
U2 - 10.1038/s41523-022-00412-2
DO - 10.1038/s41523-022-00412-2
M3 - Article
C2 - 35418131
AN - SCOPUS:85128230136
VL - 8
JO - npj Breast Cancer
JF - npj Breast Cancer
SN - 2374-4677
IS - 1
M1 - 49
ER -