SLC16A1 (Solute Carrier Family 16 Member 1)

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.

Key prognostic genes, including SLC2A1, SLC16A1, IL1A, AHSG, and ALOX15, were validated through RT-qPCR. This study highlights the molecular heterogeneity of propionate metabolism in LUAD and proposes a prognostic signature that could inform immunotherapeutic stratification.

Moreover, in MC38 and LLC mouse cancer models, pharmacologic MCT1 inhibition reprograms the immunosuppressive myeloid populations, improves CD8⁺ T cell infiltration and function, and triggers tumor regression. Therefore, these results indicate that MCT1 has the potential to be a biomarker for patients across cancer types, and to be a promising therapeutic target for enhanced cancer immunotherapy.

Both in vitro and in vivo studies demonstrate that MCT@PTO-Em NPs achieve superior tumor suppression through the synergistic interplay between pyroptosis and MPTT, while exhibiting excellent biocompatibility. This work presents a precision nanomedicine strategy that integrates molecular targeting, pyroptosis-mediated immune activation, and MPTT, offering a transformative therapeutic paradigm for HNSCC and other solid tumors.

Our study reveals the mechanism of low concentration of deguelin in ALL. It acts not through classic necroptosis, but via coordinated cell cycle arrest and a unique "metabolic trap" caused by dual inhibition of lactate synthesis and transport. These findings reposition deguelin as a promising candidate for targeted therapy against metabolic vulnerabilities in B-ALL.

Put together, our findings show that MCT4 is a promising target for the treatment of various cancers. Further integration of basic and clinical research is required to elucidate the mechanisms by which MCTs contribute to poor cancer prognosis, in turn facilitating the development of effective inhibitors.

Moreover, inhibition of Nrf2 with ML385 attenuated Cd-induced glutamine metabolism, PHGDH, MCT1, lactate production, and cell migration, while activation of Nrf2 with RTA-408 had the opposite effect...Collectively, these findings suggest that PHGDH plays a crucial role in Cd-induced lactate utilization, and the mechanism underlies the interaction between glutamine and Nrf2. This study provides insights into the mechanism of Cd-related tumorigenesis and toxicity.