Long non-coding RNA SRA1 suppresses radiotherapy resistance in esophageal squamous cell carcinoma by modulating glycolytic reprogramming.

Esophageal squamous cell carcinoma (ESCC), a highly aggressive subtype of esophageal cancer, is characterized by late-stage diagnosis and limited treatment options. Recent advancements in transcriptome sequencing technologies have illuminated the molecular intricacies of ESCC tumors, revealing metabolic reprogramming as a prominent feature. Specifically, the Warburg effect, marked by enhanced glycolysis, has emerged as a hallmark of cancer, offering potential therapeutic targets. In this study, we comprehensively analyzed bulk RNA-seq data from ESCC patients, uncovering elevated SRA1 expression in ESCC development and a poorer prognosis. Silencing of SRA1 led to a modulation of glycolysis-related products and a shift in PKM2 expression. Our findings shed light on the intricate molecular landscape of ESCC, highlighting SRA1 as a potential therapeutic target to disrupt glycolysis-dependent energy production. This metabolic reprogramming may hold the key to innovative treatment strategies for ESCC, ultimately improving patient outcomes.

Identification of Tumor Suppressor Gene LHPP-Based 5-microRNA Signature That Predicts the Early- and Midstage Esophageal Squamous Cell Carcinoma: A Two-Stage Case-Control Study in the Chinese Han Population.

OBJECTIVE: To establish a novel approach for diagnosing early- and midstage esophageal squamous cell carcinoma (ESCC). METHODS: The tumor suppressor gene phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP)-based miRNA signature was identified using next-generation sequencing and 3 biological online prediction systems. This retrospective study established and validated an ESCC prediction model using a test cohort and a validation cohort. RESULTS: Immunohistochemical staining and real-time quantitative polymerase chain reaction (RT-qPCR) results showed that LHPP protein levels were significantly lower in tissues with early- and midstage ESCC than in adjacent tissues (P < .01). Further, we confirmed that miR-15b-5p, miR-424-5p, miR-497-5p, miR-363-5p, and miR-195-5p inhibited LHPP. These 5 miRNAs were significantly elevated in the plasma of early- and midstage ESCC (P < .05). An ESCC prediction model combining these 5 miRNAs was established. Finally, in the external validation cohort, the model exhibited high discriminative value (sensitivity/specificity: 84.4%/93.3%). CONCLUSIONS: The prediction model has potential implications for diagnosis of early- and midstage ESCC.