ARF1 (ADP Ribosylation Factor 1)

Inhibition of AXL and/or Arf1 disrupted Golgi organization, tubulin acetylation and cell-surface glycosylation. Together, our findings reveal a mechanoresponsive AXL-Arf1-Golgi signaling axis that integrates matrix stiffness sensing with Golgi organization and function in breast cancer cells.

Azelastine exerts potent anticancer effects in TNBC cells via an HRH1-independent, ARF1-dependent mechanism that attenuates the Extracellular signal-regulated kinase (ERK)-Drp1 axis, and induces Drp1-dependent mitochondrial dysfunction, independent of its canonical HRH1 receptor function. This ARF1-dependent mechanism provides strong scientific rationale for the drug repositioning of azelastine as an effective therapeutic agent for ARF1-driven TNBC.

In the treatment of CC, 5-fluorouracil (5-FU) is one of the main components of chemotherapeutic combinations, but severe chemical resistance still occurs...Next, we verified that knocking down ERO1α promoted miR-451a and inhibited ARF1 expression, thus promoting ER stress and ultimately inhibiting the progression of CC. In addition, knocking down ERO1α promoted ER stress and weakened CC cell resistance to 5-FU.  Our studies revealed that ERO1α could mediate ER stress to regulate the progression of CC and 5-FU resistance through the miR-451a/ARF1 axis, which may provide new treatment directions and molecular targets for CC.

Our findings reveal that targeted downregulation of ARF1 in TAMs substantially amplifies the immune response induced by oncolytic adenoviruses, effectively reprograms these macrophages, and bolsters anti-tumor immunity. The use of oncolytic adenoviruses armed with ARF1 knockdown elements has been demonstrated to exert a significant suppressive effect on glioma growth through the concerted action of multiple pathways and effectively elicit immune memory, thereby enhancing the survival rates of tumor bearing mice and preventing tumor recurrence.

TMED2 may promote OSCC cell proliferation and inhibit apoptosis, potentially by activation of the ADP-ribosylation factor 1/ extracellular signal-regulated kinase ½ signaling pathway.

THUMPD3-AS1 inhibited ovarian cancer cell apoptosis by modulation of miR-320d/ARF1 axis. The discoveries might provide a prospective target for ovarian cancer treatment.

Furthermore, the expression of ARF was found to be strongly linked to the infiltration of various immune cell types, namely dendritic cells, macrophages, neutrophils, CD8+ T cells and B cells. These significant associations offer a solid foundation for the potential utilization of new therapeutic targets and predictive markers for the treatment of BC.

UPR-induced TF delivery to EVTFs was inhibited by Arf1 knockdown or GBF1 antagonism, confirming the role of vesicular trafficking. Our findings show that UPR activation results in increased vesicular trafficking leading to release of prothrombotic EVTFs, thus providing a mechanistic link between ER stress and cancer-associated thrombosis.

This study uncovers that ARF1-IQGAP1 interaction-mediated ERK signaling reactivation is critical for vemurafenib resistance and cancer metastasis, and that LY2835219 is a promising therapeutic agent for CRC both as a single agent and in combination with vemurafenib.

We further show that β-ionone significantly promotes ARF1 translocation to the Golgi and activates ARF1 that can be inhibited by Gγ9 and PI3Kγ depletion. Collectively, our data demonstrate that OR51E2 activates ERK1/2 through the Gβγ-PI3Kγ-ARF1 pathway that occurs spatially at the Golgi, and also provide important insights into MAPK hyper-activation in prostate cancer.

HBV utilizes a retrograde trafficking route via EEs-TGN-ER for infection that is facilitated by DOCK11 and serves to maintain cccDNA. Therefore, DOCK11 is a potential therapeutic target to prevent persistent HBV infection.