Through expression profiling, correlation assessment and survival evaluation, we identified that the FGD5-AS1/miR-22-3p axis was the most potent upstream non-coding RNA regulatory pathway for CD47 in HCC. Our findings systematically characterise the CD47-SIRPα axis as a negative prognostic indicator and an immunotherapeutic target in HCC.
The results of subcutaneous tumorigenesis experiment in nude mice indicated that the tumorigenicity of LUAD cells stably knockdown SRF was weakened and vice versa. SRF can promote the progress of LUAD by regulating lncRNA FGD5-AS1.
It was demonstrated that knockdown of FGD5-AS1 or overexpression of miR-1179 significantly reduced tumor growth in vivo. These results demonstrate a novel exosome-mediated regulatory axis, suggesting that targeting the FGD5-AS1/miR-1179/CDH3 pathway could offer new therapeutic strategies for LUAD.
FGD5-AS1 sponged miR-195-5p to mediate the upregulation of SLC7A2, overexpression of which promoted aggressiveness of OS cells. In summary, METTL16-mediated upregulation of FGD5-AS1 promotes the aggressiveness of OS though targeting of miR-195-5p/SLC7A2 axis.
In this review, we discuss the characteristics and biogenesis of exosomes and lncRNAs and how exosomal lncRNAs are involved in various processes of tumorigenesis. Our primary focus is on exosomal lncRNAs, their impact on tumor angiogenesis, and their potential as novel diagnostic markers and therapeutic targets for various cancers.
Conversely, miR-17-5p inhibition elevated lncRNA-FGD5-AS1 levels and reversed these effects.ConclusionThe findings identify the miR-17-5p/lncRNA-FGD5-AS1 regulatory axis as a novel therapeutic target for NSCLC. By integrating molecular and technological approaches, this study offers insights into precision oncology and highlights the potential for advanced RNA-based interventions.
Functional assays and transcriptome analysis following lncRNA knock-down indicated PVT1 as the master modulator of some of the most relevant BC hallmarks, such as cell proliferation, apoptosis, migration and response to hypoxia. In addition, targeted experiments identified PVT1 as a key factor in the composition of PRC2-ERα network involved in downregulation of tumor suppressor genes, including BTG2.
FGD5-AS1 promotes the stemness of HCC cells by activating the MSI2/PKD1 axis. Our study provides a new theoretical foundation for the development of novel HCC treatments.
RBM15 downregulation attenuated in vivo CRC cell proliferation by inhibiting the FGD5-AS1/HOXC10 axis. In conclusion, RBM15 promotes the FGD5-AS1/HOXC10 axis via m6A modification to promote CRC cell proliferation.
5-Fluorouracil (5-Fu) is a widely used anticancer drug for various cancers, but the development of 5-Fu resistance poses a challenge in treating cervical cancer patients...Finally, combining FGD5-AS1 silencing with 5-Fu treatments resulted in a synergistic inhibitory effect (CI < 1) on the viability of cervical cancer cells. This study reveals a FGD5-AS1-miR-130a-3p-YTHDF2 axis that could be a promising therapeutic target for overcoming 5-Fu resistance in cervical cancer.