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Although recent studies highlight the importance of histone modifications and ATP‐dependent chromatin remodelling in DNA double‐strand break (DSB) repair, how these mechanisms cooperate has remained largely unexplored. Here, we show that the SWI/SNF chromatin remodelling complex, earlier known to facilitate the phosphorylation of histone H2AX at Ser‐139 (S139ph) after DNA damage, binds to γ‐H2AX (the phosphorylated form of H2AX)‐containing nucleosomes in S139ph‐dependent manner. Unexpectedly, BRG1, the catalytic subunit of SWI/SNF, binds to γ‐H2AX nucleosomes by interacting with acetylated H3, not with S139ph itself, through its bromodomain. Blocking the BRG1 interaction with γ‐H2AX nucleosomes either by deletion or overexpression of the BRG1 bromodomain leads to defect of S139ph and DSB repair. H3 acetylation is required for the binding of BRG1 to γ‐H2AX nucleosomes. S139ph stimulates the H3 acetylation on γ‐H2AX nucleosomes, and the histone acetyltransferase Gcn5 is responsible for this novel crosstalk. The H3 acetylation on γ‐H2AX nucleosomes is induced by DNA damage. These results collectively suggest that SWI/SNF, γ‐H2AX and H3 acetylation cooperatively act in a feedback activation loop to facilitate DSB repair.

Non-alcoholic fatty liver disease (NAFLD) has emerged as a significant liver ailment attributed to factors like obesity and diabetes. While ongoing research explores treatments for NAFLD, further investigation is imperative to address this escalating health concern. NAFLD manifests as hepatic steatosis, precipitating insulin resistance and metabolic syndrome. This study aims to validate the regenerative potential of chimeric fibroblast growth factor 21 (FGF21) and Hepatocyte Growth Factor Receptor (HGFR) in NAFLD-afflicted liver cells. AML12, a murine hepatocyte cell line, was utilized to gauge the regenerative effects of chimeric FGF21/HGFR expression. Polysaccharide accumulation was affirmed through Periodic acid–Schiff (PAS) staining, while LDL uptake was microscopically observed with labeled LDL. The expression of FGF21/HGFR and NAFLD markers was analyzed by mRNA analysis with RT-PCR, which showed a decreased expression in acetyl-CoA carboxylase 1 (ACC1) and sterol regulatory element binding protein (SREBP) cleavage-activating protein (SCAP) with increased expression of hepatocellular growth factor (HGF), hepatocellular nuclear factor 4 alpha (HNF4A), and albumin (ALB). These findings affirm the hepato-regenerative properties of chimeric FGF21/HGFR within AML12 cells, opening novel avenues for therapeutic exploration in NAFLD.

Natural polysaccharides have shown promising effects on the regulation of immunity in animals. In this study, we examined the immune stimulatory effect of intranasally administered Codium fragile polysaccharides (CFPs) in mice. Intranasal administration of CFPs in C57BL/6 mice induced the upregulation of surface activation marker expression in macrophages and dendritic cells (DCs) in the mediastinal lymph node (mLN) and the production of interleukin-6 (IL-6), IL-12p70, and tumor necrosis factor-α in bronchoalveolar lavage fluid. Moreover, the number of conventional DCs (cDCs) was increased in the mLNs by the upregulation of C-C motif chemokine receptor 7 expression, and subsets of cDCs were also activated following the intranasal administration of CFP. In addition, the intranasal administration of CFPs promoted the activation of natural killer (NK) and T cells in the mLNs, which produce pro-inflammatory cytokines and cytotoxic mediators. Finally, daily administration of CFPs inhibited the infiltration of Lewis lung carcinoma cells into the lungs, and the preventive effect of CFPs on tumor growth required NK and CD8 T cells. Furthermore, CFPs combined with anti-programmed cell death-ligand 1 (PD-L1) antibody (Ab) improved the therapeutic effect of anti-PD-L1 Ab against lung cancer. Therefore, these data demonstrated that the intranasal administration of CFP induced mucosal immunity against lung cancer.

Immune stimulators are used to improve vaccine efficiency; however, they are accompanied by various side effects. In previous studies, we reported that the adhesion protein, FimH, induces immune activity; however, we did not examine any side effects in colon inflammation. FimH was administered orally or intraperitoneally ( ) to mice with dextran sulfate sodium (DSS)-induced colitis, and changes in symptoms were observed. Immune cells infiltrated into the colon after the induction of colon inflammation were analyzed using a flow cytometer. Changes in Th1 and Th17 cells that induce colitis were analyzed. Further, mesenteric lymph node (mLN) dendritic cells (DCs) activated by FimH were identified and isolated to examine their ability to induce T-cell immunity. FimH oral and administration in C57BL/6 mice did not induce inflammation in the colon; however, DSS-induced colitis was exacerbated by oral and FimH administration. FimH treatment increased immune cell infiltration in the colon compared to that in DSS colitis. Th1 and Th17 cells, which are directly related to colitis, were increased in the colon by FimH; however, FimH did not directly affect the differentiation of these T cells. FimH upregulated the CD11b CD103 DC activity in the mLNs, which produced the signature cytokines required for Th1 and Th17. In addition, isolated CD11b CD103 DCs, after stimulation with FimH, directly induced Th1 and Th17 differentiation in a co-culture of CD4 T cells. This study demonstrated the side effects of FimH and indicated that the use of FimH can aggravate the disease in patients with colitis.

Metastasis and recurrence are the main challenges in cancer treatment. Among various therapeutic approaches, immunotherapy holds promise for preventing metastasis and recurrence. In this study, we evaluated the efficacy of treating primary cancer and blocking metastasis and recurrence with photo-immunotherapeutic nanoparticles, which were synthesized using two types of charged polysaccharides. Codium fragile polysaccharide (CFP), which exhibits immune-stimulating properties and carries a negative charge, was combined with positively charged chitosan to synthesize nanoparticles. Additionally, indocyanine green (ICG), a photosensitizer, was loaded inside these particles and was referred to as chitosan-CFP-ICG (CC-ICG). Murine colon cancer cells (CT-26) internalized CC-ICG, and subsequent 808-nanometer laser irradiation promoted apoptotic/necrotic cell death. Moreover, intratumoral injection of CC-ICG, with 808-nanometer laser irradiation eliminated CT-26 tumors in mice. Rechallenged lung metastases of CT-26 cancer were inhibited by dendritic cell activation-mediated cytotoxic T lymphocyte stimulation in mice cured by CC-ICG. These results demonstrated that CC-ICG is a natural tumor therapeutic with the potential to treat primary tumors and suppress metastasis and recurrence.

Radical gastrectomy is essential for gastric cancer treatment. While guidelines advise dissecting at least 16 lymph nodes, some research suggests over 30 nodes might be beneficial. This study assessed ICG-guided robotic gastrectomy’s effectiveness in thorough lymph node dissection. We analyzed data from 393 stage II or III gastric cancer patients treated at Seoul St. Mary’s Hospital from 2016–2022. Patients were categorized into conventional laparoscopy (G1, n = 288), ICG-guided laparoscopy (G2, n = 61), and ICG-guided robotic surgery (G3, n = 44). Among 391 patients, 308 (78.4%) achieved proper lymphadenectomy. The ICG-robotic group (G3) showed the highest success rate at 90.9%. ICG-guided robotic surgery was a significant predictor for achieving proper lymphadenectomy, with an odds ratio of 3.151. In conclusion, ICG-robotic gastrectomy improves lymphadenectomy outcomes in selected gastric cancer cases, indicating a promising surgical approach for the future.

We have previously shown that inhibition of intracellular signaling pathways by treatment with quercetin induced the expression of natural killer cell group 2D (NKG2D) ligands on cancer cells and made the cells sensitive to natural killer (NK)‐cell mediated cytotoxicity. In the present study, we investigated whether epidermal growth factor receptor (EGFR) inhibitors could induce the expression of NKG2D ligands in colon cancer cells. Treatment with EGFR inhibitors predominantly increased the levels of mRNA transcripts and surface protein of UL16‐binding protein‐1 (ULBP1) in various colon cancer cells, including KM12, Caco‐2, HCT‐15, and HT‐29, which express EGFR, and increased susceptibility of these colon cancer cells to NK‐92 cells. The expression of ULBP1 was not induced by inhibitors of nuclear factor‐κB, phosphatidylinositol 3 kinase, and MAPK, but was induced by inhibitors of PKC, and the induction of ULBP1 expression with EGFR inhibitors was prevented by treatment with PMA in colon cancer cells. A transcription factor, activator protein‐2 alpha (AP‐2α), which has a suppressive effect on ULBP1 transcription, was prevented from binding to the ULBP1 promoter by treatment with EGFR inhibitors. The present study suggests that EGFR inhibitors can enhance the susceptibility to NK cell‐mediated lysis of colon cancer cells by induction of ULBP1 via inhibition of the PKC pathway. (Cancer Sci 2012; 103: 7–16)

[...]assessment showed significant improvements in hepatic gene expression of pro-inflammatory cytokines, including transforming growth factor (TGF)-β, interleukin (IL)- 1β, IL-6, IL-17A, and IL-23 after ursolic acid treatment in a dose-dependent manner. Since ursolic acid has poor permeability, it likely acts primarily on extracellular SPP1 rather than intracellular SPP1. [...]the cell type responsible for producing and secreting SPP1 in MASLD remains unclear. [...]SPP1 is well known for its pro-fibrotic effect [20], and Th17 cells contribute to liver fibrosis. Since liver fibrosis requires careful management during MASH progression, as it can lead to cirrhosis, one of the main complications of MASH, the potential anti-fibrotic effect of ursolic

Laparoscopic procedures in bariatric surgery are evolving to enhance cosmetic outcomes and minimize postoperative complications. This study demonstrates the results of bariatric surgery achieved through the application of surgical techniques derived from gastric cancer surgery. Several surgical techniques from gastric cancer surgery were implemented in bariatric surgery, including: (1) V-shaped liver retraction, (2) Reduced port surgery, (3) Intraoperative endoscopy and (4) Multi-degree-of-freedom articulating device. A single surgeon, with experience in over 1000 gastric cancer surgeries, performed consecutive bariatric surgeries starting from the initial case. The study analyzed short-term results, including operation details, postoperative complications, outcomes of weight loss, and the learning curve. A total 94 consecutive laparoscopic sleeve gastrectomy cases were performed from 2019 to 2022. The mean age of 94 patients was 35.9 ± 9.7 years, with 58 (61.7%) being female. The mean body mass index (BMI) was 40.9 ± 6.2. Type 2 diabetes was prevalent in 46.8% of the patients. On average, 3.3 ± 0.5 trocars were used per surgery. The mean estimated blood loss and hospital stay after surgery were 20.1 ± 36.3 cc and 3.3 ± 0.6 days, respectively. There were no complications reported for postoperative leakage, bleeding, or passage disturbance, and no mortality occurred. At 12 months, the mean percentage total weight loss (%TWL) and excess BMI loss (%EBMIL) were 28.5% and 79.7%, respectively. The mean operation times was 109.5 ± 27.4 min, with a plateau observed at around the 30th case. Bariatric surgery can be effectively performed by a gastric cancer expert surgeon using techniques derived from gastric cancer surgery.

Although various treatments are currently being developed, lung cancer still has a very high mortality rate. Moreover, while various strategies for the diagnosis and treatment of lung cancer are being used in clinical settings, in many cases, lung cancer does not respond to treatment and presents reducing survival rates. Cancer nanotechnology, also known as nanotechnology in cancer, is a relatively new topic of study that brings together scientists from a variety of fields, including chemistry, biology, engineering, and medicine. The use of lipid-based nanocarriers to aid drug distribution has already had a significant impact in several scientific fields. Lipid-based nanocarriers have been demonstrated to help stabilize therapeutic compounds, overcome barriers to cellular and tissue absorption, and improve in vivo drug delivery to specific target areas. For this reason, lipid-based nanocarriers are being actively researched and used for lung cancer treatment and vaccine development. This review discusses the improvements in drug delivery achieved with lipid-based nanocarriers, the obstacles that still exist with in vivo applications, and the current clinical and experimental applications of lipid-based nanocarriers in lung cancer treatment and management.