SLC16A1 (Solute Carrier Family 16 Member 1)

Pharmacological inhibition of LDHA with FX-11 synergized with anti-PD-L1 therapy, producing durable tumor regression. Collectively, these findings define LDHA-driven lactate metabolism as a key metabolic checkpoint in PCa immune evasion and provide a rationale for combining LDHA inhibition with immune checkpoint blockade to overcome immunotherapy resistance.

Monocarboxylate transporter 1 (MCT1) inhibitors disrupt their interaction, enhancing the efficacy of anti-PD-1 and antibody-drug conjugate (ADC) treatments in TNBC mouse models. Overall, our study delineates the single-cell metabolic landscape of TNBC and positions MCT1 as a promising target.

Survival analysis revealed significantly prolonged survival without systemic toxicity. Collectively, tLyP-NPs represent a promising multifunctional nanoplatform that integrates BBB penetration, TME-responsive drug release, and synergistic chemo-gene therapy for GBM treatment.

Drug sensitivity prediction and molecular docking indicated that the monocarboxylate transporter 1 (MCT1) inhibitor AZD-3965 may have therapeutic potential in this context. In general, our findings suggest that migrasome-related genes may contribute to prognostic stratification of pancreatic cancer and point to mechanisms of stroma-immune crosstalk, thereby offering exploratory avenues for personalized treatment.

This study demonstrated that SJZD alleviated CCMA by inhibiting the MCT1/lactate/H3K18Lac pathway to reduce the M2 polarization of TAMs. The elucidation of the pharmacological mechanism of SJZD provided a scientific rationale for its application in CCMA treatment.

Importantly, loss of TRIM33 accelerates tumor growth, enhances EBV reactivation, and confers resistance to lactate-transporter inhibitor. Taken together, our finding provides circulating miR-7-5p as a noninvasive biomarker and reveals TRIM33 as an integrator of lactate stress, metabolism, and viral oncogenesis, offering a novel dual-targeting therapeutic strategy.

While it is known that Warburg effects in cancers increased lactate production, followed by selection of higher MCT1 expression which enhanced cancer cell survival by exporting lactate, our findings reveal a new opportunity for killing cancer cells by increased 18β-GA sensitivities of cancer cells with higher MCT1 expression due to the Warburg effect. Thus, our results have revealed a biomarker for 18β-GA sensitivity and suggested the possibility of using Warburg effect to allow drug entry into tumor cells, and will stimulate further molecular mechanistic studies and improvements of traditional Chinese herb medicines.

Significant inverse correlations were observed between MCT1 and MCT4 expression, implying their distinct biological roles. MCT1 and MCT4 are overexpressed in CTCs from NSCLC patients, supporting their potential as prognostic biomarkers and therapeutic targets.

In vitro, XAV939 suppressed β-catenin-driven aerobic glycolysis in TNBC cells, downregulating β-catenin and glycolytic proteins, reducing glycolytic activity, and impairing aggressive phenotypes (proliferation, migration, invasion, clonogenicity).ConclusionOverall, our results highlight the crucial role of β-catenin in controlling aerobic glycolysis via regulation of key glycolytic proteins, thereby positively driving the progression and metastasis of TNBCs. Additionally, our data strongly establish that XAV939 effectively inhibits glycolytic phenotype, thereby suggesting its therapeutic potential in TNBC patients.

Functional enrichment analysis further linked the ABCC1-centred phospho-network to carcinogenesis, cell-cycle regulation, and drug resistance pathways, highlighting its systems-level role in cancer biology. From a translational perspective, our findings identify phosphosites within the ABCC1 linker domain as actionable regulatory nodes that may be exploited to modulate transporter function, offering potential strategies to overcome chemoresistance.

K-562 and HL-60 cells were treated with silibinin, an HIF-1α inhibitor, and sodium oxamate, a LDH-A inhibitor...Interestingly, the expression of MCT1, but not MCT4, was downregulated in K-562 cells after treatment. Our findings show that HIF-1α and LDH-A inhibitors not only serve as cytotoxic drugs but also regulate the expression of lactate transporter and interfere with the metabolism-related mechanisms in AML cells.

Nevertheless, a role of nuclear factor erythroid 2-related factor 2 (Nrf2) and of the proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in mediating the effect of oxidative stress and inflammation, respectively, on MCT1 and SMCT1 is suggested. So, more investigation on this subject is needed, given the fact that increased oxidative stress levels and inflammatory status are present in a series of intestinal conditions and pathologies, including CRC and IBD, which could help to establish these transporters as potential cellular targets in these diseases.