CA12 (Carbonic Anhydrase 12)

Furthermore, carbonic anhydrase 12 inhibitor U104 suppressed follicular thyroid carcinoma cell growth in a dose-dependent manner, and its combination with lenvatinib exerted synergistic antiproliferative effects. Collectively, these findings identified carbonic anhydrase 12 as a novel prognostic biomarker of follicular thyroid carcinoma and a promising therapeutic target.

And we successfully developed a predictive model to forecast the response of CRC patients to cetuximab treatment. This study will provide valuable biomarkers for CRC prognosis and help guide more effective therapeutic strategies.

Targeting IL-1α+ monocytes or IL-8 effectively inhibited tumor progression and enhanced responsiveness to immune checkpoint blockade therapy in mouse HCC models. Overall, these results revealed an intracellular regulatory role of IL-1α in modifying the pro-tumor functions of monocytes within specific tumor microenvironments and pointed to both IL-1α and its downstream IL-8 as potential diagnostic and therapeutic targets for HCC.

Development of invasion in RAS-mutant tumors is associated with significant alteration in gene expression. Expression levels of 6 genes and nodule size may predict invasion in RAS-mutant thyroid nodules, whereas chemical inhibition of CA12 may have a potential therapeutic effect in RAS-mutant tumors.

IL-1β-induced WTAP enhances CA12 mRNA stability depending on m6A modification, thus promoting chondrocyte apoptosis, inflammatory response, OxS, and ECM degradation, providing evidence to support the possibility of WTAP and CA12 as potential targets for OA treatment.

Our research offers valuable insights into the use of AF for treating NSCLC and PDAC. It highlights AF's cancer cell selectivity, establishes CA12 as a predictive biomarker for AF sensitivity, and underscores the enhanced efficacy of AF when combined with MK2206 and other therapeutics. These findings pave the way for further exploration of AF in cancer treatment, particularly in identifying patient populations most likely to benefit from its use and in optimizing combination therapies for improved patient outcomes.

In addition, SOX9 and ABCA12 cancer cells contribute to chemoresistance in human patient-derived xenografts. These findings identify a CSC-suppressing lipid metabolism pathway that can be exploited to inhibit CSCs and overcome chemoresistance.

In addition, combined CAIX/CAXII knockdown and more effective treatment with SLC-0111 reduced clonogenic survival of CMS3 modelling single cells. In conclusion, the preclinical data support the clinical approach of targeted CAIX/CAXII inhibition by showing linkage of expression with response and suggest that patients with CMS3-classified tumors would most benefit from such treatment.

Indisulam promoted an imbalance in the anti-apoptotic BCL2 and pro-apoptotic BAX protein expression. Our results demonstrate that Indisulam contributes to apoptosis via imbalance of apoptotic proteins (BAX/BCL2) and suggests a potential to overcome chemotherapy resistance caused by the regulation these proteins.

Moreover, the effect of lnc-ABCA12-3 on ESCC cells was actualized by activating the TLR4/NF-κB signaling pathway under the mediation of exosome. Taken together, the lnc-ABCA12-3 could promote the proliferation and glycolysis of ESCC, while repressing its apoptosis probably by regulating the TLR4/NF-κB signaling pathway under the mediation of exosome.