Background: Long non-coding RNAs (lncRNAs) participate in a wide range of physiological processes, and their dysregulation is prevalent in human cancers, indicating critical roles in tumorigenesis. In intermediate- to high-risk gastrointestinal stromal tumors (GISTs), resistance to tyrosine kinase inhibitors (TKIs) remains a major therapeutic challenge. Therefore, identifying lncRNAs as potential novel therapeutic targets is of considerable interest. Methods: Three paired samples of intermediate- to high-risk GIST tissues and adjacent normal tissues were subjected to transcriptome sequencing. High-content screening (HCS) was subsequently performed to identify candidate lncRNAs with significant effects on GIST cell proliferation. Loss-of-function experiments were conducted, and cell proliferation, migration, and apoptosis were evaluated using the Cell Counting Kit-8 (CCK-8) assay, colony formation assay, Transwell migration assay, and flow cytometry, respectively. In addition, in situ hybridization (ISH) was performed on 507 primary GIST tissue specimens to examine the association between CTD-2245E15.3 expression and clinicopathological features, including progression-free survival (PFS) and overall survival (OS). Results: Transcriptome sequencing revealed 2924 upregulated and 2629 downregulated lncRNAs in GIST tissues compared with adjacent normal tissues. Based on HCS results, CTD-2245E15.3 was selected for further functional analyses. CCK-8 assays demonstrated that knockdown of CTD-2245E15.3 significantly inhibited proliferation of GIST cells. Consistently, colony formation and migratory capacity were markedly reduced in the shCTD-2245E15.3 group compared with controls. Furthermore, flow cytometric analysis showed a significant increase in apoptosis following CTD-2245E15.3 silencing. ISH analysis revealed that high CTD-2245E15.3 expression correlated with adverse clinicopathological features and poorer PFS and OS. Conclusions: Our study demonstrates that CTD-2245E15.3 promotes proliferation and migration of GIST cells and is associated with poor prognosis, highlighting its potential as a therapeutic target and diagnostic biomarker.
Background: This study aimed to investigate the clinical and prognostic significance of preoperative maximum standardized uptake value (SUVmax) and GLUT-1 expression in patients with advanced gastric cancer (AGC). Methods: Medical records of patients who were diagnosed with AGC between 2018 and 2020 at Zhongshan Hospital of Fudan University (Shanghai, China) were retrospectively analyzed. Finally, 182 patients were enrolled, and for each patient, SUVmax was calculated for the primary lesion on PET/CT prior to curative surgery. A total of 165 clinical tissue specimens were collected for immunohistochemical analysis of GLUT-1 expression. Results: A total of 182 patients were divided into two groups based on their SUVmax values. The low SUVmax group comprised 92 patients. Patients with low SUVmax tended to be younger and included a higher proportion of women, with their primary tumors typically smaller or in earlier TNM stages. The median follow-up time was 52 months. The 1-, 3-, and 5-year progression-free survival (PFS) rates were 90.7%, 71.4%, and 67.0%, respectively. Among them, 33 patients experienced recurrence and metastasis, and 40 ultimately died. Log-rank analysis revealed that the low SUVmax group exhibited superior progression-free survival (PFS) and overall survival (OS). Multivariate analysis indicated that, for AGC without preoperative treatment, later stage (stage III) was independently correlated with a higher risk of recurrence (HR = 3.049; 95%CI = 1.076–8.639; p = 0.036), while the low SUVmax group exhibited a reduced risk of recurrence and mortality compared with the high SUVmax group (HR = 0.565; 95%CI = 0.326–0.979; p = 0.042). Conclusions: The clinicopathological characteristics of patients with AGC with different SUVmax values appeared significantly different. Tumor stage and SUVmax were found as independent factors affecting postoperative recurrence and death of patients with AGC.