Lysine demethylase KDM1A promotes cell growth via FKBP8–BCL2 axis in hepatocellular carcinoma

Lv, Suli; Zhao, Xuefeng; Zhang, Erlei; Yan, Yingying; Ma, Xianyun; Li, Neng; Zou, Qingli; Sun, Lidong; Song, Tanjing

doi:10.1016/j.jbc.2022.102374

Cited by 14 publications

(8 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…FKBP8 suppresses apoptosis by regulating localization and stability of Bcl-2 [ 15 ]. Cytoplasmic KDM1A could demethylate FKBP8 to increase the stability of Bcl-2 in cells of hepatocellular carcinoma [ 20 ]. In this study, FKBP8 expression was higher in TC tumor tissues than that in BTN tissues, and higher expression of FKBP8 was significantly associated with older age, lymph node metastasis, and advanced clinical stage.…”

Section: Discussionmentioning

confidence: 99%

GPX4 inhibits apoptosis of thyroid cancer cells through regulating the FKBP8/Bcl-2 axis

Dang,

Yu,

et al. 2024

CBM

View full text Add to dashboard Cite

GPX4 has attracted much attention as a key molecule of cell ferroptosis, but its role in cell apoptosis is rarely reported, and its role in apoptosis of thyroid cancer (TC) cell has not been reported. The analysis of TCGA database showed that both GPX4 and FKBP8 were highly expressed in TC tumor tissues; The expression of GPX4 and FKBP8 were positively correlated. The immunohistochemical analysis further confirmed that GPX4 and FKBP8 were highly expressed in TC tumor tissues. In addition, the high expression of GPX4 and FKBP8 were both significantly correlated with the poor prognosis of TC. Silencing GPX4 significantly inhibited the proliferation, induced apoptosis of TC cells, and reduced tumor growth in mice. The co-immunoprecipitation assay revealed a physical interaction between GPX4 and FKBP8 observed in the TC cells. Knockdown of FKBP8 significantly inhibited the proliferation and induced apoptosis of TC cells. Rescue experiments suggested that knockdown of FKBP8 could reverse the strengthens of cell proliferation and apoptosis and the higher expression of FKBP8 and Bcl-2 caused by overexpression of GPX4. Our results suggest that the GPX4/FKBP8/Bcl-2 axis promotes TC development by inhibiting TC cell apoptosis, which provides potential molecular targets for TC therapeutic strategies.

show abstract

Section: Discussionmentioning

confidence: 99%

GPX4 inhibits apoptosis of thyroid cancer cells through regulating the FKBP8/Bcl-2 axis

Dang,

Yu,

et al. 2024

CBM

View full text Add to dashboard Cite

show abstract

“…WB was performed as we described before ( 85 , 86 ). Briefly, all protein samples were prepared in 1x loading buffer (62.5 mM Tris-Cl PH6.8, 2% SDS, 10% glycerol, 5% β-mercaptoethanol, 0.002% bromophenol blue) and then separated with SDS-PAGE.…”

Section: Methodsmentioning

confidence: 99%

“…Coimmunoprecipitation was performed as we previously reported ( 85 , 86 ). Briefly, adherent cells were washed with cold PBS twice and then lysed in IPE150 buffer (20 mM Hepes pH 7.5, 150 mM NaCl, 0.5% NP40, 10% Glycerol).…”

Section: Methodsmentioning

confidence: 99%

YTHDF2 protein stabilization by the deubiquitinase OTUB1 promotes prostate cancer cell proliferation via PRSS8 mRNA degradation

Zhao,

Lv,

et al. 2024

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

“…Overexpression, amplifications, mutations, and chromosomal translocations of these genes are linked to chemotherapeutic resistance 148 . A study by Lv et al 153 showed that KDM1A can interact with and demethylate FKBP8 (FKBP prolyl isomerase 8), a protein regulating cell survival through enhancing its ability to stabilize Bcl‐2. Ramadoss et al 42 showed that KDM3A demethylates p53 protein and consequently modulates the expression of its target genes, including Bcl‐2 and p21Waf1/Cip1.…”

Section: The Mechanism Of Lysine‐specific Demethylase Mediated Drug R...mentioning

confidence: 99%

The role and prospect of lysine‐specific demethylases in cancer chemoresistance

Song

Yang

et al. 2023

Medicinal Research Reviews

View full text Add to dashboard Cite

Histone methylation plays a key function in modulating gene expression, and preserving genome integrity and epigenetic inheritance. However, aberrations of histone methylation are commonly observed in human diseases, especially cancer. Lysine methylation mediated by histone methyltransferases can be reversed by lysine demethylases (KDMs), which remove methyl marks from histone lysine residues. Currently, drug resistance is a main impediment for cancer therapy. KDMs have been found to mediate drug tolerance of many cancers via altering the metabolic profile of cancer cells, upregulating the ratio of cancer stem cells and drug‐tolerant genes, and promoting the epithelial‐mesenchymal transition and metastatic ability. Moreover, different cancers show distinct oncogenic addictions for KDMs. The abnormal activation or overexpression of KDMs can alter gene expression signatures to enhance cell survival and drug resistance in cancer cells. In this review, we describe the structural features and functions of KDMs, the KDMs preferences of different cancers, and the mechanisms of drug resistance resulting from KDMs. We then survey KDM inhibitors that have been used for combating drug resistance in cancer, and discuss the opportunities and challenges of KDMs as therapeutic targets for cancer drug resistance.

show abstract

Lysine demethylase KDM1A promotes cell growth via FKBP8–BCL2 axis in hepatocellular carcinoma

Cited by 14 publications

References 49 publications

GPX4 inhibits apoptosis of thyroid cancer cells through regulating the FKBP8/Bcl-2 axis

GPX4 inhibits apoptosis of thyroid cancer cells through regulating the FKBP8/Bcl-2 axis

YTHDF2 protein stabilization by the deubiquitinase OTUB1 promotes prostate cancer cell proliferation via PRSS8 mRNA degradation

The role and prospect of lysine‐specific demethylases in cancer chemoresistance

Contact Info

Product

Resources

About