HBP1 (HMG-Box Transcription Factor 1)

The TrxR/Trx inhibitor butaselen suppresses lung cancer by triggering ROS-induced apoptosis. This study provides a novel and effective regimen for treating lung cancer.

Suppressing the Wnt/β-catenin signaling pathway by targeting pre-miR-374b-PRKCA/HBP1 axis might represent a novel mechanism of nigericin in PC. Nigericin remained a candidate of preclinical application for PC.

HBP1 upregulation in pancreatitis mitigates pancreatic inflammatory injury; however, in the presence of oncogenic KRAS, it facilitates PanIN progression. Thus, HBP1 serves as a critical regulator in both pancreatitis and early pancreatic neoplasia, representing a potential therapeutic target for intervening pancreatitis and PanIN progression.

In addition, SOX11 upregulation reduced lenvatinib resistance in liver cancer cells by promoting ferroptosis through transcriptionally activated UBE3A expression. In summary, SOX11 upregulation promoted ferroptosis in liver cancer cells by promoting SREBF1 ubiquitination degradation through transcriptionally elevating UBE3A expression, thereby sensitizing lenvatinib-resistant liver cancer cells to lenvatinib.

Genes were identified from GeneCards and UniProt databases, differentially expressed genes were selected based on transcriptional sequencing data from wild-type and Adriamycin-resistant HL60 (HL60/WT & HL60/ADR) cell lines, and the intersection of these three sources was taken...The model accurately predicted AML prognosis and identified the UBE2L3 gene within the model as a high-risk biomarker associated with drug resistance, significantly influencing AML outcomes. The high expression of UBE2L3 is a reliable biomarker for drug resistance and poor prognosis of acute myeloid leukemia.

This study highlights the prognostic value and TME-related mechanisms of immune-stromal score signatures in ccRCC, developing a risk score model and nomogram for predicting patient prognosis.

Exosomal miR-29a-3p was then observed to migrate to the LNs and downregulate High-mobility group box transcription factor 1 (Hbp1) in Polymorphonuclear Myeloid-derived suppressor cells (PMN-MDSCs), inducing the formation of a microenvironment suitable for tumor colonization. Overall, circ-0044539 promotes HCC cell LNM abilities and induces an immune-suppressive environment in LNs through exosomes, highlighting its potential as a target for HCC LNM and HCC immunotherapy.

Mechanistically, we experimentally elucidated that variant rs1025497 might acted as an allele-specific silencer, inhibiting the expression level of oncogene RPS19 mediated by the transcription suppressive factor HBP1. Taken together, our sturdy unveils the significant role of RPS19 during CRC pathogenesis and delineates its distal regulatory mechanism mediated by rs1025497, advancing our understanding of the etiology of CRC and provided new insights into the personalized medicine of human cancer.

Additionally, the receiver operating characteristic (ROC) curve analysis of miR-29c-3p and the clinical detection/diagnostic biomarker CA125 suggests that miR-29c-3p may be conducive for clinical diagnosis or co-diagnosis of OvCa. These findings support miR-29c-3p functions as a tumor promoter by targeting its functional targets, providing new potential biomarker (s) for precision medicine strategies in OvCa.

Further double-knockdown functional assays confirmed that loss of BACH1 induced ZBTB20-mediated IFN-α production and HBP1-mediated cell-cycle arrest, indicating that BACH1-centered regulatory network may be a novel targetable vulnerability in MCL cells. Implications: BACH1 serves as a pleotropic regulator of tumor-intrinsic innate immune response and cell-cycle progression, disruption of which may offer a promising therapeutic strategy for MCL treatment.

In addition, the HBP1/TIMP3 axis promotes the sensitivity of breast cancer to radiation therapy and hormone therapy. Our study opens new perspectives on the treatment and prognosis of breast cancer.