SMTN (Smoothelin)

To explore the therapeutic role of SMTN, customized cell membrane infused biomimetic liposomes were constructed to ensure rapid delivery of SMTN siRNA specifically into HCT-116 cells, yielding significantly enhanced anti-cancer effects of irinotecan and fuzuloparib both in vitro and in vivo. To summarize, our findings revealed a novel function of SMTN in DNA damage repair and provided a therapeutic strategy of targeting SMTN to enhance the efficacy of DNA damage agents.

Targeted RNA sequencing revealed an SS18::VEZF1 gene fusion (breakpoint: exon 9-exon 2), which was confirmed by FISH (SS18). In conclusion, RNA sequencing was useful in identifying the fusion event, thereby excluding potential mimics with uncommon morphology or ambiguous immunophenotype.

These findings are supported by independent functional and clinical data. Notably, stClinic excels in label annotation through zero-shot learning and facilitates multi-omics integration by relying on other tools for latent feature initialization.

The core genes (MYL9, TAGLN, SMTN, CNN1, MYH11, MYLK, MYOCD, ACTC1, LMOD1, and TPM2) obtained in end are all lowly expressed in prostate cancer samples and are associated with hypertension, tumor metastasis, prostate tumors, and tumor aggressiveness. LMOD1 and SMTN are lowly expressed in prostate cancer and may be used as markers in prostate cancer nursing.

By addressing key diagnostic limitations and examining newer markers, our study supports a more standardized approach to diagnosing LG-ESS and underscores the value of immunohistochemical panels, particularly in fusion-negative tumors where diagnosis relies on morphological and immunohistochemical interpretation. These findings contribute critical data for improving diagnostic accuracy.

P=N/A, N=186, Completed, University Hospital Tuebingen | Recruiting --> Completed | N=135 --> 186 | Trial completion date: May 2024 --> Feb 2023 | Trial primary completion date: Jun 2022 --> Feb 2023

Fold changes for specific contractile genes in VSMCs grown in vitro for seven days in the presence (innervated) and absence (non-innervated) of sympathetic neurons were 3.5 for acta2, 6.5 for myh11, 4.19 for eln, and 4 for smtn (normalized to Tata Binding Protein (TBP)). As a result, these data suggest that sympathetic innervation promotes VSMCs' contractile gene expression and also maintains VSMCs' functional phenotype.

Key-Area Research and Development Program of Guangdong Province (No.2021B0101420006); National Natural Science Foundation of China (No.82071892, 82171920); Guangdong Provincial Key Laboratory of Artificial Intelligence in Medical Image Analysis and Application (No.2022B1212010011); the National Science Foundation for Young Scientists of China (No.82102019, 82001986); Project Funded by China Postdoctoral Science Foundation (No.2020M682643); the Outstanding Youth Science Foundation of Yunnan Basic Research Project (202101AW070001); Scientific research fund project of Department of Education of Yunnan Province(2022J0249). Science and technology Projects in Guangzhou (202201020001;202201010513); High-level Hospital Construction Project (DFJH201805, DFJHBF202105).

A total of 235 DEGs and 12 hub genes were identified in this study, which may contribute to a further understanding of the molecular mechanisms of the development and progression of PCa, and provide new candidate targets for the diagnosis and treatment of the malignancy.

The sensitivity of smoothelin in CL seems rather low, but no data is available to assess its specificity. On a molecular level, the most common mutually exclusive aberration in CL affects HMGA2, followed by chromosome 1p deletions and MED12 mutations.

ARHGAP8 was found in both multivariate analyses and in analyses that combined gene expression and clinical information. This approach provides both mechanistic information and, when combined with predictive clinical information, good evidence that the identified genes are significant biomarkers of processes involved in CRC progression and survival.

Molecular docking revealed the binding of JS-K to TAGLN and shTAGLN-2.15 cells were resistant to JS-K cytotoxicity, suggesting that TAGLN could be an important target in JS-K anti-HBV-positive liver cancer cells. These proteomic findings could shed new insights into mechanisms underlying the effect of JS-K against HBV-related HCC.