CANX (Calnexin)

This study highlights probable hub genes, drugs targeting them, and associated pathways perturbed by SARS-CoV-2 NSP6. Galectin3 (LGALS3) upregulated in both heart and brain after COVID-19 infection is reported to be influencing all the ten hallmarks of cancer. Our bioinformatics and systems study hints probable effect of COVID-19 infection in cancer incidence and warrants in-depth studies for present scenario of long and recurrent COVID-19.

Molecular docking studies confirmed strong binding affinity of verteporfin (ITGA4 inhibitor, docking score=-16.0 kcal/mol) and ebselen (MPO inhibitor) to their respective targets, suggesting potential therapeutic strategies to overcome chemotherapy resistance. This study establishes a robust 13-gene exosome-based prognostic signature for AML risk stratification and identifies novel immunomodulatory mechanisms mediated by exosome-driven Treg polarization.

We propose a robust MHCRG-based gene signature, validated through both bioinformatic analyses and in vitro functional experiments. These findings offer translational potential for improving risk stratification and guiding immunotherapy in CC patients.

Rescue experiments validated the essential function of the hsa_circ_0007991/miR-505-3p/CANX pathway in HCC. hsa_circ_0007991 is upregulated in HCC and closely associated with tumor proliferation and immune evasion by regulating the miR-505-3p/CANX axis.

We showed that a candidate compound fluzoparib effectively suppressed HBC-positive liver cancer cells in vitro and in vivo. Overall, this study underscores the crucial role of CANX and its regulatory mechanisms in promoting HBC-mediated liver cancer progression and reveals the therapeutic potential of targeting CANX in HBV infection-caused liver cancer.

These findings suggested that CALR promotes the progression of ESCC by regulating ER stress and mitochondrial function to mediate ATP production, cytoskeletal remodeling, cell proliferation and apoptosis through CANX and PDIA3. Knockdown CALR significantly inhibited tumor‑associated fibroblast infiltration and is a potential drug target for ESCC.

Overall, this work represents the first systematic analysis of how the absence of individual APPM components, knocked out in a single cell line under controlled conditions, affects the peptidome. This approach could facilitate the creation of predictive tools capable of prioritizing HLA-bound peptides likely to be presented when presentation defects occur, such as in cancer and viral infections.

Mechanistically, circCANX recruits the tumor suppressor protein P53 (P53) mRNA and RNA helicase upstream frameshift 1 (UPF1) to form a ternary complex, which mediates P53 mRNA degradation through nonsense-mediated mRNA decay (NMD) process. Together, this study reveals an important circCANX-mediated regulatory mechanism in COPD, and provides new insights into the potential of circRNA-based drug and biomarker development for COPD.

Notably, when combined with temozolomide (TMZ), CANX knockdown extended the lifespan of GBM-bearing mice. Additionally, our studies revealed that the classic calcium inhibitor nimodipine (ND) decreased CANX expression and thus enhanced the sensitivity to TMZ. Our findings indicate that CANX functions as an oncogene in GBM. We also characterize the CANX/MEK/ERK/BNIP3 mitophagy pathway, provide new insights into the molecular mechanism of GBM drug resistance, and identify a therapeutic target.

In vivo, SH514 effectively inhibited the proliferation of MM tumors, showing much better antitumor efficacy than the clinical drug lenalidomide, and exhibited no significant toxicity. Thus, these IRF4 inhibitors could serve as promising leads for the development of novel anti-multiple myeloma agents.

In conclusion, this study suggested that CANX may promote the malignant progression of glioma through PI3K/AKT/mTOR signaling pathway and play an important role in glioma immune escape. Therefore, CANX may be a valuable therapeutic target for glioma.