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Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE290774 | GEO | 2025/07/31

REPOSITORIES: GEO

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Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [cutandtag]

Project description:The primate-restricted KRAB zinc finger protein (KZFP) ZNF93 represses a subset of L1 transposable elements (TEs) that propagated in the human ancestral genome some 20 to 12 million years ago and have all become transposition-incompetent due to inactivating mutations. Here, we demonstrate that these L1 integrants encode a highly genotoxic endonuclease, and that ZNF93 also represses other full-length L1 integrants via indirect effects as well as APOBEC3B. Consistent with the exquisite sensitivity of single-stranded DNA to attack by both the L1 endonuclease and the cytidine deaminase, ZNF93 expression peaks in S phase and correlates with cell proliferation. ZNF93 is induced in most cancers, and ZNF93-depleted cells exhibit defects in DNA synthesis and activation of the replication and DNA damage checkpoints. These results suggest a model whereby ZNF93 is a major guardian of genome integrity subverted by cancer cells to escape L1-mediated epigenetic surveillance and achieve a proper balance of APOBEC3B-induced tumor heterogeneity and overall genome stability.

2025-08-01 | GSE290773 | GEO

Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [RNA-seq_2]

2025-08-01 | GSE290771 | GEO

Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [RNA-seq_1]

2025-08-01 | GSE290770 | GEO

Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [RNA-seq_3]

2025-08-01 | GSE290772 | GEO

Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B

Project description:Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B

| PRJNA1230070 | ENA

Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [cutandtag]

Project description:Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [cutandtag]

| PRJNA1230089 | ENA

Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [RNA-seq_1]

Project description:Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [RNA-seq_1]

| PRJNA1230087 | ENA

Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [RNA-seq_3]

Project description:Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [RNA-seq_3]

| PRJNA1230088 | ENA

Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [RNA-seq_2]

Project description:Cancer cells subvert ZNF93 to escape surveillance by L1 epigenetic sentinels and control APOBEC3B [RNA-seq_2]

| PRJNA1230072 | ENA

PD-L1 methylation restricts PD-L1/PD-1 interactions to control cancer immune surveillance.

Project description:Immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) or programmed cell death 1 ligand 1 (PD-L1) have enabled some patients with cancer to experience durable, complete treatment responses; however, reliable anti-PD-(L)1 treatment response biomarkers are lacking. Our research found that PD-L1 K162 was methylated by SETD7 and demethylated by LSD2. Furthermore, PD-L1 K162 methylation controlled the PD-1/PD-L1 interaction and obviously enhanced the suppression of T cell activity controlling cancer immune surveillance. We demonstrated that PD-L1 hypermethylation was the key mechanism for anti-PD-L1 therapy resistance, investigated that PD-L1 K162 methylation was a negative predictive marker for anti-PD-1 treatment in patients with non-small cell lung cancer, and showed that the PD-L1 K162 methylation:PD-L1 ratio was a more accurate biomarker for predicting anti-PD-(L)1 therapy sensitivity. These findings provide insights into the regulation of the PD-1/PD-L1 pathway, identify a modification of this critical immune checkpoint, and highlight a predictive biomarker of the response to PD-1/PD-L1 blockade therapy.

| S-EPMC10219601 | biostudies-literature

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