KDM4B down-regulation facilitated breast cancer cell stemness via PHGDH upregulation in H3K36me3-dependent manner
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature..
Despite recent advances have been made in clinical treatments of breast cancer, the general prognosis of patients remains poor. Therefore, it is imperative to develop a more effective therapeutic strategy. Lysine demethylase 4B (KDM4B) has been reported to participate in breast cancer development recently, but its exact biological role in breast cancer remains unclear. Here, we observed that KDM4B was down-regulated in human primary BRCA tissues and the low levels of KDM4B expression were correlated with poor survival. Gain- and loss-of-function experiments showed that KDM4B inhibited the proliferation and metastasis of breast cancer cells. Besides, knockdown of KDM4B promoted the epithelial-mesenchymal transition (EMT) and cell stemness in breast cancer cells. Mechanistically, KDM4B down-regulates PHGDH by decreasing the enrichment of H3K36me3 on the promoter region of PHGDH. Knockdown of PHGDH could significantly reversed proliferation, migration, EMT, and cell stemness induced by KDM4B silencing in breast cancer cells. Collectively, we propose a model for a KDM4B/PHGDH axis that provides novel insight into breast cancer development, which may serve as a potential factor for predicting prognosis and a therapeutic target for breast cancer.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:479 |
|---|---|
| Enthalten in: |
Molecular and cellular biochemistry - 479(2024), 4 vom: 20. Apr., Seite 915-928 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Wang, Xin-Yu [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Breast cancer |
|---|
| Anmerkungen: |
Date Completed 15.04.2024 Date Revised 15.04.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1007/s11010-023-04777-1 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM357519736 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM357519736 | ||
| 003 | DE-627 | ||
| 005 | 20240415232851.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1007/s11010-023-04777-1 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1376.xml |
| 035 | |a (DE-627)NLM357519736 | ||
| 035 | |a (NLM)37249813 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Wang, Xin-Yu |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a KDM4B down-regulation facilitated breast cancer cell stemness via PHGDH upregulation in H3K36me3-dependent manner |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 15.04.2024 | ||
| 500 | |a Date Revised 15.04.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. | ||
| 520 | |a Despite recent advances have been made in clinical treatments of breast cancer, the general prognosis of patients remains poor. Therefore, it is imperative to develop a more effective therapeutic strategy. Lysine demethylase 4B (KDM4B) has been reported to participate in breast cancer development recently, but its exact biological role in breast cancer remains unclear. Here, we observed that KDM4B was down-regulated in human primary BRCA tissues and the low levels of KDM4B expression were correlated with poor survival. Gain- and loss-of-function experiments showed that KDM4B inhibited the proliferation and metastasis of breast cancer cells. Besides, knockdown of KDM4B promoted the epithelial-mesenchymal transition (EMT) and cell stemness in breast cancer cells. Mechanistically, KDM4B down-regulates PHGDH by decreasing the enrichment of H3K36me3 on the promoter region of PHGDH. Knockdown of PHGDH could significantly reversed proliferation, migration, EMT, and cell stemness induced by KDM4B silencing in breast cancer cells. Collectively, we propose a model for a KDM4B/PHGDH axis that provides novel insight into breast cancer development, which may serve as a potential factor for predicting prognosis and a therapeutic target for breast cancer | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Breast cancer | |
| 650 | 4 | |a H3K36me3 | |
| 650 | 4 | |a KDM4B | |
| 650 | 4 | |a PHGDH | |
| 650 | 4 | |a Stemness | |
| 650 | 7 | |a KDM4B protein, human |2 NLM | |
| 650 | 7 | |a EC 1.14.11.- |2 NLM | |
| 650 | 7 | |a Jumonji Domain-Containing Histone Demethylases |2 NLM | |
| 650 | 7 | |a EC 1.14.11.- |2 NLM | |
| 700 | 1 | |a Li, Hong-Ming |e verfasserin |4 aut | |
| 700 | 1 | |a Xia, Ran |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Xiang |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Xing |e verfasserin |4 aut | |
| 700 | 1 | |a Jin, Tong-Zhao |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Hong-Sheng |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Molecular and cellular biochemistry |d 1973 |g 479(2024), 4 vom: 20. Apr., Seite 915-928 |w (DE-627)NLM000008133 |x 1573-4919 |7 nnns |
| 773 | 1 | 8 | |g volume:479 |g year:2024 |g number:4 |g day:20 |g month:04 |g pages:915-928 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1007/s11010-023-04777-1 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 479 |j 2024 |e 4 |b 20 |c 04 |h 915-928 | ||