MACC1-AS1 (MACC1 Antisense RNA 1)

Moreover, MACC1-AS1 contributes to therapeutic resistance, conferring reduced sensitivity to chemotherapeutic agents such as 5-fluorouracil (5-FU), oxaliplatin, gemcitabine, and cisplatin, as well as to combination regimens including 5-fluorouracil and oxaliplatin (FOLFOX). This review provides an overview of the current knowledge surrounding MACC1-AS1 and highlights its potential as both a biomarker and a therapeutic target for future translational research.

In this overarching review, we explore the significance of MACC1-AS1 as a potential cancer treatment target and biomarker. This study can potentially play an important role in the advancement of the field and confirm its potential clinical applicability.

Rescue assays indicated that repressed SCLC cell growth caused by MACC1-AS1 knockdown could be reserved by miR-579-3p repression or NOTCH1 overexpression. In brief, lncRNA MACC1-AS1 boosted SCLC cell growth via sequestering miR-579-3p and mediating NOTCH1-pathway.

These findings suggested that the long non-coding RNA MACC1-AS1 could play a significant role in the ability of pancreatic cancer cells to evade iron-mediated ferroptosis induced by gemcitabine. This discovery holds promise for developing clinical therapeutic strategies to combat chemotherapy resistance in pancreatic cancer.

Moreover, binding of DDX5 to the core promoter results in local recruitment of the transcription factor SP-1, thus enhancing MACC1 transcription. Our findings reveal a molecular mechanism by which MACC1-AS1 cis-regulates MACC1 transcription by interacting with the distal promoter region and delivering DDX5 to the core-promoter of the gene.

Our study suggests that in each cell type, there is a balance of interactions between certain lncRNAs and miRNAs. Disrupting the balance would eventually affect the expression of miRNA-targeted genes and cell proliferation.

IFN-γ affected PC properties by MACC1-AS1/MACC1 axis via AKT/mTOR signaling pathway, which provides novel insight for candidate targets for treating PC.

We also identified that the low expression of MEG3, LINC01963, and LINC00261 and the high expression of MACC1-AS1, LINC00462, LINC01559, and UCA1 were significantly correlated with worse survival in pancreatic cancer patients. Further research on these lncRNAs will provide new clues that could potentially improve the early diagnosis, prognostic prediction, and personalized treatments of patients with pancreatic cancer.