Effectively targeting cancer stem cells to treat cancer has great therapeutic prospects. However, the effect of microRNA miR-17/MKL-1 on gastric cancer stem cells has not been studied yet. This study preliminarily explored the mechanism of miR-17/MKL-1 in gastric cancer stem cells. Many previous reports have indicated that microRNA and EMT regulated cancer stem cell characteristics, and miR-17 and MKL-1 were involved as a critical gene in migration and invasion in the EMT pathway. Through RT-PCR, Western Blot, flow cytometry, immunofluorescence, sphere formation xenograft tumor assays and drug resistance, the role of miR-17-5p and MKL-1 on promoting stem cell-like properties of gastric cancer were verified in vivo and vitro. Next, MKL-1 targets CD44, EpCAM, and miR -17-5p promoter verified by luciferase assay and ChIP. Besides, the TCGA database analysis found that both miR-17-5p and MKL-1 increased in gastric cancer, and the prognostic survival of the MKL-1 high expression group was reduced. It is found that MKL-1 promotes expression by targeting miR-17, CD44 and EpCAM promoters. Besides, the TCGA database analysis found that both miR-17-5p and MKL-1 increased in gastric cancer, and the prognostic survival of the MKL-1 high expression group was reduced. These findings reveal new regulatory signaling pathways for gastric cancer stem cells, thus it give new insights on potential early diagnosis and/or molecular therapy for gastric cancer.

Background: Cancer patients are at increased risk of novel coronavirus disease 2019 (COVID-19). Currently, surgeries for cancer patients with COVID-19 are generally suggested to be properly delayed.Case presentation: We presented a 69-year-old Chinese female colon cancer patient with COVID-19, the first case accepted the surgical treatment during the pandemic in China. The patient developed a fever on January 28, 2020. After treatments with Ceftriaxone and Abidol, her fever was not moderated yet. A repeat chest computed tomography (CT) scan showed significantly exacerbated infectious lesions with a positive result for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nucleic acid. An abdomen CT scan indicated the tumor of ascending colon with local wrapped changes. She was diagnosed with ‘Severe novel coronavirus pneumonia’ and ‘Incomplete bowel obstruction: Colon cancer?’. After actively anti-inflammatory and anti-viral therapies, a right colectomy with lymph node dissection was performed on March 11, followed by a pathological examination. The patient successfully recovered from COVID-19 pneumonia and incomplete bowel obstruction after surgery without any postoperative related complications and was discharged on the 9th day after operation. Significant degeneration, necrosis and slough of focal intestinal and colonic mucosal epithelial cells were observed under microscope. No surgeons, nurses or anesthetists in our team were infected with SARS-CoV-2.Conclusions: It is meaningful and imperative to share our experience of protecting health care personnels from SARS-CoV-2 infection and providing references for optimizing treatment of cancer patients, at least for the operative intervention with absolute necessity or surgical emergency, during the outbreak of COVID-19.

[This corrects the article DOI: 10.7150/ijbs.57338.].

Pancreatic cancer has nearly doubled in incidence over the past two decades, becoming one of the deadliest types of malignancy in humans, with poor prognosis. With advances in modern medicine, the 5‑year survival rate for pancreatic cancer has increased from 1x10¹⁴ microorganisms that influence the development of pancreatic cancer through immune modulation and metabolites. Circadian rhythms, as a conserved molecular feedback loop, regulate cell metabolism and immune function, and their dysregulation is associated with metabolic disorders and tumor progression. Circadian rhythm disruption not only affects the gut microbiota and its metabolites but also accelerates pancreatic cancer progression through mechanisms such as promoting inflammation, immune suppression and drug resistance. The present review summarizes the impact of circadian rhythm dysregulation on the gut microbiota and its metabolites, specific microbiota associated with pancreatic cancer and their mechanisms in tumor progression and aims to deepen the understanding of the role of gut microbiota in pancreatic cancer treatment, providing a theoretical basis for future therapeutic strategies.

Objectives Nasopharyngeal carcinoma (NPC) is an aggressive malignancy with high rates of morbidity and mortality, largely because of its late diagnosis and metastatic potential. Lactate metabolism and protein lactylation are thought to play roles in NPC pathogenesis by modulating the tumor microenvironment and immune evasion. However, research specifically linking lactate-related mechanisms to NPC remains limited. This study aimed to identify lactate-associated biomarkers in NPC and explore their underlying mechanisms, with a particular focus on immune modulation and tumor progression. Methods To achieve these objectives, we utilized a bioinformatics approach in which publicly available gene expression datasets related to NPC were analysed. Differential expression analysis revealed differentially expressed genes (DEGs) between NPC and normal tissues. We performed weighted gene coexpression network analysis (WGCNA) to identify module genes significantly associated with NPC. Overlaps among DEGs, key module genes, and lactate-related genes (LRGs) were analysed to derive lactate-related differentially expressed genes (LR-DEGs). Machine learning algorithms can be used to predict potential biomarkers, and immune infiltration analysis can be used to examine the relationships between identified biomarkers and immune cell types, particularly M0 macrophages and B cells. Results A total of 1,058 DEGs were identified between the NPC and normal tissue groups. From this set, 372 key module genes associated with NPC were isolated. By intersecting the DEGs, key module genes, and lactate-related genes (LRGs), 17 lactate-related DEGs (LR-DEGs) were identified. Using three machine learning algorithms, this list was further refined, resulting in three primary lactate-related biomarkers: TPPP3, MUC4, and CLIC6. These biomarkers were significantly enriched in pathways related to "immune cell activation" and the "extracellular matrix environment." Additionally, M0 and B macrophages were found to be closely associated with these biomarkers, suggesting their involvement in shaping the NPC immune microenvironment. Conclusion In summary, this study identified TPPP3, MUC4, and CLIC6 as lactate-associated clinical modelling indicators linked to NPC. linked to NPC, providing a foundation for advancing diagnostic and therapeutic strategies for this malignancy.