Api5 a new cofactor of estrogen receptor alpha involved in breast cancer outcome

Basset, Céline; Bonnet-Magnaval, Florence; Navarro, Marina Garcia-Jove; Touriol, Christian; Courtade, M; Piégay, Hervé; Garmy‐Susini, Barbara; Lacazette, Éric

doi:10.18632/oncotarget.17281

Cited by 14 publications

(18 citation statements)

References 36 publications

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“…As a ligand of TLR4, apoptosis inhibitor 5 (API5) is an apoptosis inhibitory protein that prevents apoptosis induced by the transcription factor E2F1 and interacts with a nuclear factor involved in apoptotic DNA fragmentation 55 – 57 . For instance, API5 is associated with diseases, including adenocarcinoma and cervical cancer 58 , 59 . It can be released from tumor cells and functions as a DAMP protein activating immune cells 57 .…”

Section: Damp Proteins Released From Dying Cellsmentioning

confidence: 99%

Interactions between tumor-derived proteins and Toll-like receptors

et al. 2020

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Damage-associated molecular patterns (DAMPs) are danger signals (or alarmins) alerting immune cells through pattern recognition receptors (PRRs) to begin defense activity. Moreover, DAMPs are host biomolecules that can initiate a noninflammatory response to infection, and pathogen-associated molecular pattern (PAMPs) perpetuate the inflammatory response to infection. Many DAMPs are proteins that have defined intracellular functions and are released from dying cells after tissue injury or chemo-/radiotherapy. In the tumor microenvironment, DAMPs can be ligands for Toll-like receptors (TLRs) expressed on immune cells and induce cytokine production and T-cell activation. Moreover, DAMPs released from tumor cells can directly activate tumor-expressed TLRs that induce chemoresistance, migration, invasion, and metastasis. Furthermore, DAMP-induced chronic inflammation in the tumor microenvironment causes an increase in immunosuppressive populations, such as M2 macrophages, myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs). Therefore, regulation of DAMP proteins can reduce excessive inflammation to create an immunogenic tumor microenvironment. Here, we review tumor-derived DAMP proteins as ligands of TLRs and discuss their association with immune cells, tumors, and the composition of the tumor microenvironment.

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Section: Damp Proteins Released From Dying Cellsmentioning

confidence: 99%

Interactions between tumor-derived proteins and Toll-like receptors

et al. 2020

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“…Triple-negative breast cancer is highly malignant, aggressive, resistant to chemotherapy, and has a poor prognosis[ 3 – 5 ]. However, the molecular mechanisms of breast cancer remain unclear[ 6 – 8 ].…”

Section: Introductionmentioning

confidence: 99%

ALG3 Is Activated by Heat Shock Factor 2 and Promotes Breast Cancer Growth

et al. 2018

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BackgroundPrevious research found that ALG3 is associated with cervical cancer, but the role of ALG3 in breast cancer was still unknown.Material/MethodsThe expression of ALG3 in breast carcinoma tissues was determined by immunochemistry. The ability of cellular proliferation, migration, and invasion was determined by CCK-8 assay, wound healing migration assay, and cell invasion assays, respectively. The binding between HSF2 and promoter of ALG3 was determined by ChIP assay.ResultsThere was an increased expression of ALG3 in breast cancer tissues compared to normal breast tissues (p<0.05). High expression of ALG3 was significantly correlated with poor OS (p<0.05). ALG3 expression was significantly increased in cancer samples with advanced stages (stage III/IV) compared with those in the early stages of disease (stage I/II) (p<0.05). The staining intensity of ALG3 was significantly correlated to the tumor grade (grades 2–3 versus 1, p<0.05). Silencing ALG3 or HSF2 inhibited the proliferation, migration, and invasion abilities of MCF-7 cells. Silencing ALG3 retarded the growth of MCF-7 cells in vivo.ConclusionsSilencing ALG3 inhibited MCF-7 cells growth in vitro and in vivo. HSF2 activated ALG3 and promoted the growth of breast carcinoma.

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“…Reduced and low levels of Api5 are associated with the increase in cell death in various cancers. Knockdown of Api5 resulted in the reduction in in vivo tumorogenicity in cancer cells 14 .…”

Section: Introductionmentioning

confidence: 99%

“…High levels of Api5 provide cancer cells the ability to evade immune response mediated cell death 6 . In breast cancers, Api5 interacts with the estrogen receptor to promote proliferation 14 . It has also been reported that Api5 promotes metastasis in breast cancers 14 .…”

Section: Introductionmentioning

confidence: 99%

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Interplay between p300 and HDAC1 regulate acetylation and stability of Api5 to regulate cell proliferation

Sharma

Lahiri

2021

Sci Rep

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Api5, is a known anti-apoptotic and nuclear protein that is responsible for inhibiting cell death in serum-starved conditions. The only known post-translational modification of Api5 is acetylation at lysine 251 (K251). K251 acetylation of Api5 is responsible for maintaining its stability while the de-acetylated form of Api5 is unstable. This study aimed to find out the enzymes regulating acetylation and deacetylation of Api5 and the effect of acetylation on its function. Our studies suggest that acetylation of Api5 at lysine 251 is mediated by p300 histone acetyltransferase while de-acetylation is carried out by HDAC1. Inhibition of acetylation by p300 leads to a reduction in Api5 levels while inhibition of deacetylation by HDAC1 results in increased levels of Api5. This dynamic switch between acetylation and deacetylation regulates the localisation of Api5 in the cell. This study also demonstrates that the regulation of acetylation and deacetylation of Api5 is an essential factor for the progression of the cell cycle.

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Api5 a new cofactor of estrogen receptor alpha involved in breast cancer outcome

Cited by 14 publications

References 36 publications

Interactions between tumor-derived proteins and Toll-like receptors

Interactions between tumor-derived proteins and Toll-like receptors

ALG3 Is Activated by Heat Shock Factor 2 and Promotes Breast Cancer Growth

Interplay between p300 and HDAC1 regulate acetylation and stability of Api5 to regulate cell proliferation

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