LASP1 (LIM And SH3 Protein 1)

[This retracts the article DOI: 10.3727/096504017X14850151453092.].

[This retracts the article DOI: 10.2147/OTT.S116509.].

Moreover, patients with high expression of both IFIT3 and LASP1 have a poorer prognosis. In conclusion, IFIT3 promotes LNM in ESCC through the LASP1/FAK/ERK axis, and IFIT3 is a potential therapeutic target for LNM in ESCC.

Furthermore, we found that, similar to what was described in other cell types, NK cells require CLASP1/2 and AKAP350 for efficient nucleation of microtubules at the Golgi. Overall, this study uncovers the role of CLASP1/2 in the maturation of the lytic IS in NK cells and presents evidence supporting the contribution of GDMTs in this process.

Further analysis reveals that U2AF2 regulates circCLASP1 biogenesis. Collectively, these findings demonstrate that circCLASP1 promotes BC progression and an immunosuppressive microenvironment via the CCT2/GLI1/SNAIL axis, highlighting its potential as a prognostic biomarker and therapeutic target for BC.

Moreover, we demonstrate a positive correlation between high expression of CXCR4 and low expression of LASP1 and EIF4A1 via gene correlation targeted analysis, which is consistent with the result among the triple-negative breast cancer patients. Our results suggest that CXCR4 can be used as a biological factor to predict the prognosis of BC patients, especially those with triple-negative breast cancer, and is also a tumor marker with potential value in the future treatment of BC.

FNBP1 knockdown significantly suppressed tumor growth in the subcutaneous model and reduced the number of lung nodules in the metastasis model. In conclusion, FNBP1, regulated by the RBM15B-m6A-IGF2BP2 axis, promotes GBM progression by interacting with LASP1 to activate Smad3-mediated glycolysis.

CLASP1 and possibly the microtubule machinery in broader sense seem involved in protection of HNSCC cells against radiation-induced DNA damage. This newly identified mechanism provides an outlook for novel treatment approaches in HNSCC.

CXCR4-targeted radioligands enabled both imaging and inhibition of NEPC tumors in vivo. These findings highlight the CXCR4-LASP1-G9a-SNAIL axis as a key regulator of epigenetic and transcriptional reprogramming in NEPC transdifferentiation and support its therapeutic targeting in aggressive NEPC.

DAB2 could bind to LASP1 to participate in NSCLC development, involving the regulatory mechanism of TGF-β/Smad pathway.

The ChIP-seq results showed that NFE2L3 regulated the expression of LASP1 and thus activated the AKT/GSK3β signalling pathway. In summary, our results suggest that NAT10 mediates ac4C acetylation of NFE2L3 mRNA, promotes its mRNA stability, regulates the LASP1-AKT/GSK3β/β-catenin axis and promotes the progression of renal clear cell carcinoma.

KMT2A::LASP1 fusion was retrospectively detected in her bone marrow at the initial presentation of AID-like symptoms, suggesting the involvement of leukemia cells in her AID-like symptoms. Immediately after starting chemotherapy, the patient sequentially developed leukemic cell lysis pneumopathy (LCLP), which was successfully overcome by the continuation of chemotherapy under intensive respiratory support, thus suggesting a possible association of her AID-like symptoms with the development of LCLP.