LINC01133 (Long Intergenic Non-Protein Coding RNA 1133)

Furthermore, PRR5 abundance was particularly enriched and correlated with that of phosphorylated ERK in samples from patients with TNBC. Our results highlight cross-talk between mTORC2 and ERK signaling downstream of LINC01133 and PRR5 that may be therapeutically targeted to treat TNBC.

In vivo studies confirmed that either overexpression of LINC01133 or inhibition of miR-199a-5p suppresses gastric adenocarcinoma cell growth. In summary, LINC01133 re-activation may serve as a potential therapeutic strategy for inhibiting metastasis in gastric adenocarcinoma.

The dual character of LINC01133 in tumor biology further demonstrates its prospective therapeutic value, but complete elucidation of its mechanisms of action requires further investigation. This study establishes LINC01133 as a multifaceted lncRNA, supporting context-specific strategies in targeting its pathways, and calls for expanded research to harness its full potential in oncology.

The downregulation of LINC01133 was mediated by m6A modification, catalyzed by METTL3 and recognized by YTHDF2, causing half-life reduction and accelerated degradation of LINC01133. Our findings revealed the downregulation of LINC01133 in ER+ breast cancer and provided novel insight to the role of METTL3/YTHDF2/LINC01133/IGF2BP2 axis in ER+ breast cancer, which might offer a novel perspective in the design and development of novel anticancer drugs.

We identified a novel risk signature consisting of four PRlncRNAs, which is an independent prognostic indicator for patients with COAD. This PRlncRNA risk signature is potentially relevant for immunotherapy and could serve as a therapeutic target for COAD.

Decreased serum LINC01133 had considerable diagnostic potential, and the joint detection of LINC01133, CEA, and CA19-9 might be a more efficient diagnostic strategy for GC patients. Reduced LINC01133 served as a prognostic biomarker to predict poor GC survival.

LINC01133 bound with actin-related protein 3 (Arp3), the complex reduced SPP1 mRNA degradation which increased SPP1 mRNA level, ultimately leading to PDAC proliferation. This research revealed a novel mechanism of PDAC development and provided a potential prognosis indicator that may benefit PDAC patients.

Knocking down miR-30b-5p expression or up-regulating FOXA1 expression was able to reverse siRNA-LINC01133 inhibitory effect of tumor cell malignant behavior. LINC01133 promoted FOX1 expression by competitively binding miR-30b-5p, which attenuated the targeting inhibitory effect of miR-30b-5p on FOXA1 and ultimately promoted proliferation and invasive migration of NSCLC cells.

LINC01133 interacted with miR-30d-5p to modulate MARCKS expression, contributes to promoted cell proliferation, migration, invasion, and inhibited cell apoptosis in vitro, and promoted tumor growth in vivo. These findings could provide possible therapeutic targets in view of LUSC treatment in the future.

Survival analysis showed that, regardless of TMB risk, patients with MC and a high-risk score consistently had a poor overall survival (OS). The m7G-related lncRNA prognostic signature has potential value for the prognosis of mucinous colonic adenocarcinoma.

These findings posit that propofol induces LINC01133 expression, leading to the inhibition of CRC progression. This revelation offers a novel perspective on propofol's antitumor properties and underscores the potential of LINC01133 as a promising therapeutic target for CRC.

A higher CEBPB could also indicate a higher IC50 of sorafenib in patients with cancer. Moreover, we confirmed that LINC01133 could form a triple complex with FUS and FSP1 to increase the mRNA stability of FSP1.