DDX11-AS1 (DDX11 Antisense RNA 1)

Strikingly, functional studies reveal that LINC01134 acts as a crucial oncogenic driver and its depletion suppresses proliferation, migration, and invasion while sensitizing cells to triaptosis via MTM1-mediated PI(3)P catabolism. Collectively, our study confirms that triaptosis is a therapeutically targetable signaling in HCC and proposes LINC01134 as a biomarker and therapeutic target, offering new insights into lncRNA-mediated regulation of cell death for precision oncology.

Critically, inhibition of miR-1183 rescued the suppressive effects of DDX11-AS1 knockdown on glioma tumorigenic phenotypes and restored E2F7 expression levels. This study demonstrates that lncRNA DDX11-AS1 promotes glioma progression by regulating the miR-1183/E2F7 axis, indicating a potential therapeutic target for glioma.

In conclusion, the small protein DDX11-AS1-ORF, encoded by DDX11-AS1, plays a crucial role in the development of colorectal cancer by promoting tumor proliferation, migration, and angiogenesis through the activation of VEGFA and the p38-MAPK signaling pathway. These findings provide a novel potential target for molecular targeted therapy in colorectal cancer.

Furthermore, DDX11-AS1 was revealed to be transcriptionally regulated by NRF1. DDX11-AS1, a NRF1-induced lncRNA, facilitates HCC development by upregulating CA9 expression and activating the MEK/ERK signaling cascade.

Subsequently, these five lncRNAs were validated using the independent validation set. In summary, this investigation successfully discerned five lncRNAs closely associated with the oncogenesis of HCC, thereby shedding light on their potential utility as diagnostic or therapeutic targets for this formidable disease.

The promoting effect of DDX11-AS1 on BC cells was enhanced by miR-30c-5p silencing and reduced by treatment with MTDH inhibitors. Collectively, the above results suggest that the DDX11-AS1/miR-30c-5p/MTDH axis could be associated with the progression of BC and that DDX11-AS1 could be a potential biomarker and therapeutic target for BC.

In summary, our study unveils the potent role of DDX11-AS1 as an enhancer of sorafenib resistance, inhibiting sorafenib-induced ferroptosis through the activation of the Nrf2-Keap1 pathway in HCC. These findings offer a promising therapeutic strategy to overcome resistance and effectively treat HCC.

CONCLUSIONS This study delves into the intricate correlation between ARGs and immune cell infiltration in HCC, culminating in the development of a novel prognostic model reliant on 11 ARGs-associated lncRNAs. Furthermore, our findings highlight ANXA5 as a promising target for immune regulation in HCC, offering new perspectives for immune therapy in the context of HCC.

According to the results of Western blotting, after interfering with the expression of DDX11-AS1 in BC cells, there were changes in the expressions of molecular markers for EMT. In BC, the expression of lncRNA DDX11-AS1 is up-regulated, which promotes the proliferation, migration and invasion of BC cells by regulating EMT.

DNA damage repairing ability was also modulated by the change of DDX11-AS1 expression. LncRNA DDX11-AS1 promotes DNA damage repair to enhance PTX resistance in LUAD.