SREBP1 is a well-known transcript factor regulating lipogenesis. It has been reported to play an important role in tumor progress in recent years. However, the roles of SREBP1 in differentiated thyroid cancer (DTC) are uncertain. Based on this, we aimed to investigate the expression of SREBP1 and the influence of SREBP1 on DTC patients. qRT-PCR and immunohistochemistry were used to detect the expression of SREBPs in DTC tissues and the adjacent normal tissues. The following methods, including the MTS, colony-forming assay, flow cytometry and Hoechst staining were used to detect the biological function of thyroid cancer cells based on SREBP1 interference or not. the expression of SREBP1 was significantly different among DTCs, thyroid nodules and the adjacent normal tissues. Briefly, SREBP1 was upregulated follow with the malignancy, but there was no significant difference of SREBP2 between thyroid nodules and the adjacent normal tissues. Further, the ROC curve showed that SREBP1 has higher diagnostic value than SREBP2. SREBP1 expression was significantly related to the tumor size and lymph node metastasis in DTCs. In vitro, the proliferation of thyroid cancer cells was suppressed obviously after interfered with SREBP1, and the apoptotic cells was increased. Further, SREBP1 expression was also associated with the short-term efficacy of levothyroxine in DTC patients. this is the first time to report that SREBP1 is an oncogene and a pro-proliferation factor in thyroid cancer, indicating that SREBP1 may serve as a potential biomarker and therapeutic target in thyroid cancer.

Glioma refers to a tumor of the brain and central nervous system, which is characterized by high incidence, high mortality and high recurrence rate. Although the association between glioma and the repressor element silencing transcription factor (REST) has been reported by numerous studies, the complicated regulatory mechanisms underlying REST remain unknown. REST is a transcriptional repressor that undergoes alternative splicing to produce splicing variants when transcribed. Previous studies have demonstrated that alternative splicing may serve a role in the outcome of glioma. The present review discussed the mutual relationship among REST, REST4 and glioma. It was concluded that increased REST expression in glioma may be associated with poor prognosis; and REST4, an AS variant of REST, also functions to regulate glioma by suppressing REST. In addition, the present review discussed the regulation of REST and its target genes in glioma, and identified factors that induce REST alternative splicing, particularly in glioma. These findings suggest that REST may be considered a prognostic factor, which can be predictive of patient outcome.

Background: While an association between gut microbiota composition and thyroid cancer (TC) has been observed, the directionality and causality of this relationship remain unclear. Methods: We conducted a bidirectional two-sample Mendelian randomization (MR) analysis to investigate the causal effect between gut microbiota composition and TC. Gut microbiota data were derived from a diverse population encompassing various ethnicities (n = 18,340 samples), while TC data were sourced from an European population (n = 218,792 samples). Instrumental variables, represented by single nucleotide polymorphisms (SNPs), were employed to assess the causal relationship using multiple MR methods, including inverse-variance weighting (IVW), weighted median, weighted mode, MR-Egger, and simple mode. F-statistics and sensitivity analyses were performed to evaluate the robustness of the findings. Results: Our investigation identified a comprehensive set of 2934 instrumental variables significantly linked to gut microbiota composition (p < 1 × 10^-5). The analysis illuminated notable candidates within the phylum Euryarchaeota, including families Christensenellaceae and Victivallaceae, and genera Methanobrevibacter, Ruminococcus2, and Subdoligranulum, which emerged as potential risk factors for TC. On the other hand, a protective influence against TC was attributed to class Betaproteobacteria, family FamilyXI, and genera Anaerofilum, Odoribacter, and Sutterella, alongside order Burkholderiales. Further enhancing our insights, the integration of 7 instrumental variables from TC data (p < 1 × 10^-5) disclosed the regulatory potential of one family and five genera. Notably, the genus Coprobacter innocuum group (p = 0.012, OR = 0.944) exhibited the highest probability of regulation. Our meticulous analyses remained free from significant bias, heterogeneity, or horizontal pleiotropy concerns. Conclusion: Through a bidirectional two-sample Mendelian randomization approach, we elucidated a potential bidirectional causal relationship between gut microbiota composition and TC. Specific microbial taxa were associated with an increased risk or conferred protection against TC. These findings advance our understanding of the complex interplay between the gut microbiota and TC pathogenesis, offering new insights into the therapeutic potential of modulating the gut microbiota for managing TC.

Aim: To investigate the association between SNPs in DNA damage response pathways and toxicities following 131I radiotherapy of differentiated thyroid cancer (DTC). Materials & methods: We identified 22 functional SNPs of genes in DNA damage response pathways. MassArray was used to sequence SNP genotypes in 203 DTC patients. Hardy–Weinberg equilibrium and the associations between the two alleles of each SNP and toxicity reactions were evaluated using χ2 analysis. Results: Ataxia-telangiectasia mutated (ATM) rs620815 T-allele carriers were at increased risk of 131I radiation-induced gastrointestinal reaction compared with C allele carriers. TNFα rs1800629 GA genotype may increase the incidence of neck pain compared with GG genotype. Furthermore, TNFα rs1800629, ATM rs11212570, NF-κβ rs230493, and TGF-β rs1800469, rs2241716 were associated with throat pain following 131I radiotherapy. Conclusion: The identified SNPs might serve as novel biomarkers for DTC treated with 131I radiotherapy.