Jiangchao Li

Metastasis remains the leading cause of cancer-related mortality and arises from ongoing interactions between malignant cells and their surrounding microenvironment. Among host factors, platelets and neutrophils have emerged as key regulators of metastatic potential. Growing evidence indicates that their coordinated activity—particularly through platelet–neutrophil aggregates（PNAs） and related mixed-cell complexes—forms an important but underrecognized pathway that promotes immune escape, vascular adaptation, and preparation of distant metastatic sites. This combination alters many critical steps in the spreading process. It includes survival within the circulation, evading the immune response, adhesion to the vessel wall and egress, and shifting target tissues. These are the result of collaborative mechanisms such as the use of soluble signaling factors, cell-cell adhesion, the NET-inflammatory response linked to coagulation, and the more persistent changes conferred by EVs and metabolism. Despite substantial progress in defining these mechanisms, important challenges limit clinical translation. Blood count–based platelet and neutrophil markers are not consistently used to assess metastatic risk across cancer types; the factors that control when and how neutrophils change functional states within tumors remain unclear; and therapeutic strategies that target platelet–neutrophil cooperation must carefully balance antimetastatic efficacy with risks such as bleeding and weakened host defense. In this review, we integrate current evidence on platelet–neutrophil–tumor interactions into a unified framework that connects biological mechanisms with clinically measurable indicators and therapeutic entry points. We examine emerging approaches to reduce metastasis supported by platelet–neutrophil interactions and NET-associated processes, consider how these strategies may complement existing cancer treatments, and emphasize the potential of combined biomarker models—such as integrating platelet measures with the neutrophil-to-lymphocyte ratio（NLR）—to improve prognostic assessment and guide future clinical validation.

Cervical cancer remains one of the leading causes of cancer-related mortality among women worldwide. The prognosis of cervical cancer is poor due to persis

Intestinal adenomas are premalignant lesions that develop into colorectal cancer (CRC), yet the metabolic pathways underlying their malignant transformation remain poorly characterized. Using targeted metabolomics via ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS), we found that serum levels of the bioactive lipid metabolite 14,15-epoxyeicosatrienoic acid (14,15-EET) were dramatically elevated in Apc^Min/+ adenoma model mice as early as pre-adenoma stages, compared to C57BL/6 controls. The results were also consistent in adenomas and CRC patients. ELISA data and bioinformatics analyses revealed both elevated serum 14,15-EET levels and upregulated cytochrome P450 2J2 (CYP2J2) expression in tumor. Functional studies showed that 14,15-EET accelerates adenoma growth in vivo, and promotes proliferation, migration, and invasion in vitro by activating AKT (Ser473)/ERK1/2 signaling and inducing epithelial-mesenchymal transition (EMT). Its early elevation in premalignant lesions, and relative molecules 14,15-EET/CYP2J2 represents a novel strategy for disrupting adenoma-carcinoma transition, and offering new biomarker for CRC prevention.

Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer-related death worldwide. Many studies have attempted to elucidate the role of cytochrome 450 (CYP450) polymorphisms in cancer susceptibility and tumor progression. However, the function of Cytochrome P450 Family 2 Subfamily S Member 1(CYP2S1), a member of the CYP450 family, in CRC remains unclear. Here, we constructed APC^Min/+;CYP2S1^-/- mice. We found that CYP2S1 knockout in APC^Min/+ mice led to an increased number of adenomas, accelerated tumor progression and enhanced proliferation and angiogenesis of adenomas. Consistently, in vitro experiments demonstrated that CYP2S1 silencing enhanced the proliferation, migration and invasion of CRC cells. Furthermore, CYP2S1 knockout promoted the nuclear translocation of β-catenin in intestinal epithelial cells of APC^Min/+ mice and in cancer cells, it also activated Wnt and modulated P53 signaling pathways, upregulating metastasis associated in colon cancer 1 (MACC1), which accelerated cancer cell proliferation and invasion. Database analysis revealed that CYP2S1 was upregulated in colorectal cancer and positively associated with better prognosis. In conclusion, these findings suggest that CYP2S1 represents a promising biomarker and therapeutic target for improving the prognosis and treatment of colorectal cancer.

In eukaryotes, the ribosomal small subunit (40S) is composed of 18S rRNA and 33 ribosomal proteins. 18S rRNA has a special secondary structure and is an indispensable part of the translation process. Herein, a special sequence located in mammalian 18S rRNA named Poly(G)₇box, which is composed of seven guanines, was found. Poly(G)₇ can form a special and stable secondary structure by binding to the translation elongation factor subunit eEF1D and the ribosomal protein RPL32. Poly(G)₇box was transfected into cells, and the translation efficiency of cells was inhibited. We believe that Poly(G)₇box is an important translation-related functional element located on mammalian 18S rRNA, meanwhile the Poly(G)₇ located on mRNA 5' and 3' box does not affect mRNA translation.

Cancer immunotherapy has been proven to be clinically effective in multiple types of cancers. Lymphocyte function-associated antigen 1 (LFA-1), a member of the integrin family of adhesion molecules, is expressed mainly on αβ T cells. LFA-1 is associated with tumor immune responses, but its exact mechanism remains unknown. Here, two kinds of mice tumor model of LFA-1 knockout (LFA-1^−/−) mice bearing subcutaneous tumor and Apc^Min/+;LFA-1^−/− mice were used to confirm that LFA-1 knockout resulted in inhibition of tumor growth. Furthermore, it also demonstrated that the numbers of regulatory T cells (Treg cells) in the spleen, blood, mesenteric lymph nodes were decreased in LFA-1^−/− mice, and the numbers of Treg cells in mesenteric lymph nodes were also decreased in Apc^Min/+;LFA-1^−/− mice compared with Apc^Min/+ mice. LFA-1 inhibitor (BIRT377) was administered to subcutaneous tumor-bearing LFA-1^+/+ mice, and the results showed that the tumor growth was inhibited and the number of Treg cells was reduced. The analysis of TIMER tumor database indicated that LFA-1 expression is positively associated with Treg cells and TNM stage. Conclusively, this suggests that LFA-1 knockout would inhibit tumor growth and is correlated with Treg cells. LFA-1 may be one potential target for cancer immunotherapy.

Alterations in the gut microbiome have been linked to obesity and type 2 diabetes, in epidemiologic studies and studies of fecal transfer effects in germ-free mice. Here, we aimed to identify the effects of specific gut microbes on the phenotype of mice fed a high-fat diet (HFD). After eight weeks of HFD feeding, male C57BL/6J mice in the HFD group ranking in the upper and lower quartiles for body weight gain were considered obese prone and obese resistant, respectively. 16S rRNA gene sequencing was used to determine the composition of the intestinal microbiota, and fecal transplantation (FMT) was conducted to determine whether the microbiota plays a causal role in phenotypic variation. Ruminococcaceae_UCG-013 was more abundant in the gut microbes of mice with a lean phenotype than in those with an obese phenotype. Ruminococcaceae_UCG-013 was identified as the most significant biomarker for alleviating obesity by random forest analysis. In a correlation analysis of serum parameters and body weight, Ruminococcaceae_UCG-013 was positively associated with serum HDL-C levels and negatively associated with serum TC, TG, and LDL-C levels. To conclude, Ruminococcaceae_UCG-013 was identified as a novel microbiome biomarker for obesity resistance, which may serve as a basis for understanding the critical gut microbes responsible for obesity resistance. Ruminococcaceae_UCG-013 may serve as a target for microbiome-based diagnoses and treatments in the future.