ATG9B (Autophagy Related 9B)

CBX2 promotes cisplatin resistance in OC via SIAH2-mediated β-catenin stabilization and ATG9B-dependent autophagy activation. Overall, our study reveals a hitherto undocumented role of CBX2 in mediating DDP resistance, providing insights for potential therapeutic biomarkers to overcome DDP resistance in OC.

CD31+ KHE cells can replicate human KHE in murine models, offering a valuable tool for studying pathogenesis. Our findings also suggest a potential mechanism of sirolimus action in treating KHE, warranting further investigation into novel therapeutic strategies.

This highlights the complexity of the epigenetic regulation of ATG2B, ATG4D, ATG9A and ATG9B genes in CRC. Further large-scale studies will contribute to discovering the exact influences of ATG methylation in CRC carcinogenesis and thereby may thereby provide novel targets and biomarkers for this lethal illness.

Thus, we analyzed autophagy-related genes using public databases to investigate a novel prognostic autophagy signature for glioblastoma patients who received temozolomide (TMZ) and RT...We also validated the higher expression of these genes and autophagy flux in TMZ-resistant glioblastoma cells than in TMZ-sensitive cells. Therefore, the autophagy-related gene set could serve as an independent prognostic biomarker for predicting the response to standard therapy in glioblastoma patients.

We developed and validated a robust nomogram for predicting RFS in cT1 ccRCC patients after nephrectomy, offering valuable insights for individualized patient management.

CDK5 knockdown partially attenuated the ATG9B-4-induced increase in proliferation and migration in liver cancer cells. ATG9B-4 deteriorated the proliferation and migration of liver cancer cells in an ARNTL-CDK5 pathway-dependent manner.

ATG9B is highly likely to mutate during RT and ATG9B mutation correlates to higher CEA and CA19-9 levels and patients show poor prognosis. The online version contains supplementary material available at 10.1007/s12291-023-01177-6.

Recent findings, however, including structural, proteomic, and biochemical analyses, have provided new insights into its function in the expansion of the phagophore membrane. In this review, we aim to understand various aspects of ATG9 (in invertebrates and plants)/ATG9A (in mammals), including its localization, trafficking, and other functions, in nonneuronal cells and neurons by comparing recent discoveries related to ATG9/ATG9A and proposing directions for future research.Abbreviation: AP-4: adaptor protein complex 4; ATG: autophagy related; cKO: conditional knockout; CLA-1: CLArinet (functional homolog of cytomatrix at the active zone proteins piccolo and fife); cryo-EM: cryogenic electron microscopy; ER: endoplasmic reticulum; KO: knockout; PAS: phagophore assembly site; PtdIns3K: class III phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; RB1CC1/FIP200: RB1 inducible coiled-coil 1; SV: synaptic vesicle; TGN: trans-Golgi network; ULK: unc-51 like autophagy activating kinase; WIPI2: WD repeat domain, phosphoinositide interacting 2.

Blocking ATG9B's scramblase activity or depleting ANXA1 decreased niche macrophages and hindered tumor progression. Thus, IL-33 is released from live CSCs via LOs to promote the differentiation of alternatively activated macrophage, with potential relevance to other settings of inflammation and tissue repair.

Whole uteri were collected on days 1, 4, and 8 of pregnancy and from ovariectomized mice injected with vehicle, progesterone, or 17β-estradiol...The Atg9 isoforms exhibited distinct subcellular localizations in UECs and may play different roles in autophagy. Notably, human uterine cells exhibited reduced ATG9B expression, suggesting that this suppression may be due to epigenetic regulation.

Knockdown of CPNE7 reversed the induction of the autophagy pathway by rapamycin and reduced the number of autophagosomes. Depletion of CPNE7 attenuated the malignant proliferation of CRC cells and enhanced the chemosensitivity of CRC cells to 5-fluorouracil.

The combination of Rapamycin with Cisplatin potentializes the inhibition of Ca9-22 cell proliferation. Identifying gene-gene interaction (GGI) networks provided a comprehensive view of the drug's mechanism and connected the studied tumorigenesis processes to potential functional interactions of various kinds (physical interaction, co-expression, genetic interactions etc.). In conclusion, Rapamycin shows promise as a clinical agent for managing Ca9-22 gingiva carcinoma cells.