Adhesions within the abdominal cavity develop in as many as 90 % of individuals following abdominal surgery. However, the true adhesive condition of patients can only be ascertained during the second surgery. We conducted a prospective, non-randomized study to assess the anti-adhesion properties of purified starch in patients who had undergone colorectal surgery in the past and then needed a subsequent surgical intervention. Adhesion scores have been prospectively recorded in operation notes since January 2020 when patients underwent a second surgery. Patients who had received purified starch during their initial surgery constituted the purified starch group, while those who had not received anti-adhesion medical materials were the control group. The main objectives of the study were to evaluate the extent and severity of adhesions as primary outcomes, while secondary outcomes included measuring blood loss, operation time, and postoperative complications. We analyzed the data of 101 patients, with 61 in the purified starch group and 40 in the control group. In multivariate analysis, adhesion severity (Odds ratio, 0.20, 95 % confidence interval 0.08–0.54, P < 0.01) and adhesion area scores (Odds ratio, 0.13, 95 % confidence interval 0.04–0.45, P < 0.01) were significantly lower in the purified starch group than in the control group. There was no significant difference in operation times, blood loss, and postoperative complications between the two groups. Purified starch is a safe and effective anti-adhesion material that can significantly reduce the severity and extent of adhesion after colorectal surgery.

Colorectal cancer (CRC) is the third most common type of cancer worldwide, and distant metastasis is frequently noted at diagnosis or follow-up. Notably, some patients with CRC can present with distant organ metastasis without any nodal involvement, which was defined as direct distant organ metastasis (DDOM). In this study, we evaluated the prognostic significance of DDOM for patients with CRC. This study included 325 patients who had undergone primary colorectal cancer resection between August 2008 and December 2021. The patients with and without DDOM were compared (Kaplan-Meier analysis) in terms of overall survival (OS) and time to recurrence. Furthermore, the patients' clinicopathological risk factors and protective factors were analyzed (multivariate Cox proportional hazards model). Of the 325 patients, 65 (20%) had DDOM (Direct⁺ group) and 260 (80%) did not (Direct^- group). The Kaplan-Meier analysis revealed that OS was significantly better in the Direct⁺ group than in the Direct^- group (p < 0.01). A subgroup analysis by CRC stage was performed; for the patients with non-stage-IV CRC, the rate of OS was significantly higher in the Direct⁺ group than in the Direct^- group (p = 0.02). However, DDOM did not affect the OS of the patients with stage IV CRC. The multivariate analysis indicated DDOM, left colon tumor location, and postoperative adjuvant chemotherapy were significant protective factors for disease-related mortality in the patients with non-stage-IV CRC; by contrast, body mass index, curative resection, and postoperative adjuvant chemotherapy were identified to be significant protective factors in the patients with stage IV CRC. DDOM appears to be significantly associated with improved OS in patients with non-stage-IV CRC but not in those with stage IV CRC. Furthermore, the time to cancer recurrence may not vary significantly between patients with DDOM and those without it.

Colorectal cancer (CRC) progression and therapy resistance are driven in part by metabolic reprogramming and the persistence of cancer stem-like cells (CSCs). The seven in absentia homolog 2 (SIAH2)/with-no-lysine kinase 1 (WNK1) signaling axis has emerged as a potential regulator of these processes, yet its functional role in CRC metabolism and tumor–stroma crosstalk remains incompletely understood. Integrated analyses of The Cancer Genome Atlas–Colon Adenocarcinoma (TCGA-COAD) and Gene Expression Omnibus (GEO, GSE17538) datasets revealed significant upregulation of SIAH2 and WNK1 in CRC tissues, with strong positive correlations to glycolysis- and hypoxia-associated genes, including PFKP, LDHA, BPGM, ADH1A, ADH1B, and HIF-1α. Single-cell and clinical profiling further demonstrated preferential enrichment of SIAH2 in undifferentiated, stem-like tumor cell populations. Functional studies across multiple CRC cell lines showed that SIAH2 silencing suppressed proliferation, clonogenic growth, tumor sphere formation, and cell-cycle progression, whereas SIAH2 overexpression exerted opposite effects. Seahorse extracellular flux analyses established that SIAH2 promotes glycolytic capacity and metabolic flexibility. At the protein level, SIAH2 regulated glycolytic enzymes and WNK1/hypoxia-inducible factor-1α (HIF-1α) signaling, effects that were amplified by cancer-associated fibroblast (CAF)-derived conditioned medium. CAF exposure enhanced SIAH2 expression, CSC spheroid growth, and resistance to fluorouracil, leucovorin, and oxaliplatin (FOLFOX) chemotherapy, whereas SIAH2 depletion effectively abrogated these effects. Collectively, these findings identify the SIAH2/WNK1 axis as a central metabolic regulator linking glycolysis, CSC maintenance, and microenvironment-driven therapy resistance in CRC, highlighting its potential as a therapeutic target.