TBX2 (T-Box Transcription Factor 2)

The combined assessment of PAX9, HK10, TBX2, and CYFRA21-1 provides significant diagnostic and prognostic value in ovarian carcinoma, with HK10 showing particularly high sensitivity. These markers could play a crucial role in the early detection and management of ovarian carcinoma.

Peptide deformylase regulates CYP11B2 expression and aldosterone production. The CALB1-calcium signaling pathway may mediate the effects of peptide deformylase on aldosterone overproduction.

Impressively, piroctone olamine was also effective in PDAC patient-derived organoids. Together, our data demonstrate the potential of piroctone olamine to be repurposed for treating TBX2-/3-dependent PDAC.

NFIC inhibited the migration and proliferation of SKOV3 cells, while TBX2 promoted it; NFIC functioned through TGFβ1 and PTEN, and their inhibition promoted the migration and proliferation of SKOV3 cells. NFIC inhibits the progression of epithelial ovarian cancer by regulating the balance of PTEN/TGFβ1/EGR1/BRD4 and SP1/EZH2 to suppress the TBX2/MMPs signaling pathway.

Through nebulization, 20%b-3C-2P12 mediated high Tbx2 mRNA expression in the lungs of silicosis mice, effectively restoring lung functions. This study not only establishes a strategy for development of LNP-like O-LhPAEs but also provides promising candidates for highly safe, efficient, and spleen-selective mRNA delivery and nebulization treatment of silicosis.

Understanding the complex molecular networks that TBX2 is involved in to exert its oncogenic functions is important because it may reveal potential therapeutic strategies for targeting TBX2 in TBX2-dependent cancers. This minireview discusses TBX2's involvement in cancer signalling, its regulatory partners, and its impact on cancer progression and resistance to therapy.

Notably, we report that SP2509, an allosteric inhibitor of the demethylase-independent function of LSD1 (a TBX2-interacting protein in the COREST complex) disrupts both TBX2-LSD1 and TBX2-GR protein-protein interactions, revealing a unique mode of SP2509 action in CRPC. Taken together, our study identifies the TBX2-driven AR- to GR- signaling switch as a molecular mechanism underlying enzalutamide resistance and provides key insights into a potential therapeutic approach for targeting this switch by disrupting TBX2-GR and TBX2-LSD1 protein-protein interactions.

Circ_0060927 downregulation inhibited CRC progression by regulating the miR-331-3p/TBX2 axis, which might offer a potential treatment target for CRC.

Niclosamide, piroctone olamine, and pyrvinium pamoate are promising, cost-effective therapeutic agents for the treatment of TBX2/TBX3-dependent cancers.

Interestingly, silence FSP1 could reverse TBX2-mediated ferroptosis inhibition and tumor-promoting effect. TBX2-FSP1 axis inhibits ferroptosis and enhances the Cisplatin resistance, which will provide an important theoretical basis and potential solution for the clinical treatment of EC.

Additionally, elevated expression of TBX2 is associated with resistance to DNA-damaging chemotherapeutic agents, such as cisplatin, carboplatin and doxorubicin. Moreover, TBX2 knockdown significantly enhanced cervical cancer cell sensitivity to cisplatin in vitro (P<0.05). These findings highlight TBX2 expression as a potential predictive biomarker for recurrence amongst patients with intermediate- to high-risk stage IB-IIB cervical cancer receiving adjuvant TP chemotherapy post-radical hysterectomy.

Our research provided sufficient evidence that TBX2 subfamily might play an inhibitory role in malignancy progression of lung cancer, which is promising to shed light on discovering a novel reliable cancer marker for prognosis of lung cancer patients.