TUBB3 (Tubulin beta 3 class III)

In this study, we hypothesize that SB-216 and Veru-111 (related novel compounds) inhibit cell growth via suppression of oncogenic βIII- and βIVb-tubulin subtypes and mitochondria function via suppression of BRD4, the most active BET protein...Our data demonstrates that SB-216 effectively inhibits PDAC cell growth through inhibiting oncogenic microtubules and mitochondrial function. This novel approach simultaneously targets two hallmarks of cancer and patient demise.

A panel comprising seven key IPF genes was identified, which may have diagnostic and prognostic value for IPF. A comprehensive analysis of the Dgidb database revealed potential drugs that may be antitumor agents against IPF, such as Lygodii Spora, Smilacis Glabrae Rhizoma, and Aloe.

DTX1 overexpression suppresses the M2 polarization of TAM, which is overturned by TUBB3 overexpression. These findings provide the first evidence indicating that DTX1 mediates the ubiquitination of TUBB3 in KCs to block the AKT signaling and the M2 polarization of TAM in HCC.

Such tools provide an important first step in identifying novel mediators of disease pathogenesis and likely hold the key for the discovery of potential treatment targets for BKPyVAN in the future.

This multi-omics, public data-driven synthesis delineates a coherent network of genomic, epigenomic, transcriptomic, and structural vulnerabilities, offering a rational framework for therapeutic targeting of cholangiocarcinoma. This study reveals novel bile duct-associated variations that expand our understanding of cholangiocarcinoma pathogenesis and provide potential targets for precision medicine approaches.

Functional studies reveal that HOMER3 overexpression enhances ECM stiffness, type I collagen deposition, and Aβ accumulation in the tumor stroma, leading to tumor growth and aggressiveness, while HOMER3 knockdown reduces ECM stiffness, disrupts collagen composition, and increases sensitivity to docetaxel. These findings establish HOMER3 as a pivotal regulator of OSCC malignancy and chemoresistance, providing novel insights into its role in orchestrating the tumor microenvironment and identifying it as a promising therapeutic target for OSCC.

PTTG1 is highly expressed in various NB cells. Interfering with PTTG1 induces autophagy, thereby inhibiting SK-N-SH cell proliferation and promoting differentiation.

Lastly, controlling the pore size to 100-250 μm further increased cell coverage to >70%, breaking through previous plateau and upregulating TUBB3 maturity marker. Additionally, certain key factors are seen to synergistically codominate in determining cell growth.

Mechanistically, TUBB3 promoted G2/M transition via p21/Cyclin B1 and enhanced invasiveness through Cortactin/JNK activation.ConclusionTUBB3 overexpression predicts poor prognosis in gastric cancer. It drives proliferation via cell cycle regulation and metastasis through invadopodia formation, suggesting its potential as a therapeutic target.

These findings highlight the complexity of chemoresistance mechanisms. The characterized cell line panel represents a valuable resource for future studies aimed at understanding and overcoming drug resistance in bladder cancer, suggesting that personalized therapeutic approaches may be necessary.

TUBB3 may play an essential role in the development and progression of UC. TUBB3 was associated with the basal subtype. TUBB3 could be a potential therapeutic target and biomarker in UC.

Specifically, changes in microtubule interactions with the integrin-linked kinase-integrin-β1 axis contributed to a reduced invasive potential. The unique properties of these analogs suggest their potential for dual-action therapy combining tumor growth inhibition with metastasis prevention.