WNT5A (Wnt Family Member 5A)

We identified 12 signature hub genes associated with CRLM by using both scRNA-seq and bulk RNA-seq analysis. Further, we revealed the vital role of TCF21, which promotes CRLM by regulating WNT5A in CRC metastasis. The revelations have illuminated the pivotal function of the TCF21-WNT5A pathway in the development of colorectal cancer, indicating possible avenues for therapeutic intervention aimed at preventing and managing the spread of CRC.

Collectively, impaired pancreatic insulin secretion by aberrant Wnt5a/β-catenin activation may underlie the hyperglycemia associated with PDAC. Our finding provides insights into the unique molecular mechanism of pancreatic cancer-associated hyperglycemia, paving the way for the identification of potential biomarker and therapeutic targets for this condition.

Therapeutically, targeting ROR1 via endothelial-specific Adno-Associated Virus (AAV) knockdown or the antibody-drug conjugate Zilovertamab vedotin (VLS-101) normalizes vasculature, improves temozolomide delivery, and sensitizes tumors in glioblastoma organoids and xenografts. These findings highlight the ROR1-WNT5A axis as a promising target in glioblastomas treatment.

Acupuncture may alleviate AS by modulating osteogenic pathways and gut microbiota, thus reducing inflammation and pathological ossification.

WNT5A inhibits steroidogenesis via the PI3K/AKT pathway in granulosa cells. Our findings suggest that increased WNT5A may be attributed to inflammation and may result in endocrine dysregulation in PCOS patients.

Our results showed that HOXA-AS3 might promote glioma progression via regulating hsa-miR-542-5p/HOXA1 and WNT5A.

NCAPD2 enhanced the proliferation and metastasis of EC cells by promoting glycolysis through Wnt5A-mediated activation of the Notch pathway. This finding not only revealed the critical role of the NCAPD2/Wnt5A axis in EC but also provided a potential therapeutic target for EC treatment.

PRMT2 not only induced M2-like polarization of tumor-associated macrophages (TAMs) but also impaired anti-tumor T cell responses by promoting CD4+/CD8+ T cell dysfunction. In conclusion, our findings position PRMT2 as a multifaceted therapeutic target that simultaneously addresses tumor intrinsic malignancy and microenvironmental immunosuppression in CRC.

These genes were differentially expressed in MSC cultures derived from patients and healthy donors, as well as between patients grouped according to their response to therapy. Therefore, WNT proteins and β-catenin can be considered potential markers to assess the state of the tumor niche.

IVM was administered to endocrine-resistant breast cancer cell lines, MCF-7/LCC2 (tamoxifen resistant) and MCF-7/LCC9 (fulvestrant resistant), to evaluate its influence on cell proliferation, invasion, and EMT-related mechanisms. In conclusion, IVM inhibits the Wnt signaling pathway associated with EMT in the metastasis of endocrine-resistant breast cancer cells. These insights underscore the potential of repurposing IVM for endocrine-resistant breast cancer patients.

Pan-cancer analysis revealed that MMP11+ mCAFs are present across various cancer types, including breast cancer, lung adenocarcinoma, gastric cancer, and colorectal cancer. These findings provide insights into the heterogeneity of CAFs and their regulatory role in tumor progression, offering new potential therapeutic targets for CAF-targeted treatments with broad applicability across cancers.

Targeting the ROR2-YAP/TEAD axis presents a promising therapeutic approach to overcome trastuzumab resistance in HER2-positive cancers, offering a potential strategy for enhancing treatment efficacy and improving clinical outcomes.