Synovial sarcoma of the viscera (lung and jejunum): a case report.

We report the case of a woman nearing 70 years old who was admitted to the hospital with a complaint of "epigastric distension for 1 month". Her main signs and symptoms were progressive abdominal distension and occasional abdominal pain. Computed tomography suggested an abdominal mass. She had a surgical history of synovial sarcoma (SS) of the lungs. After admission, she was diagnosed with jejunal SS following a puncture biopsy and laparoscopic surgery. This disease usually occurs in the soft tissues of the limbs, and it is extremely rare for SS to originate in the jejunum. The morphologic heterogeneity of SS overlaps with other tumors and makes the diagnosis particularly difficult. Imaging studies usually lack specificity; however, measuring multiple immunohistochemical markers can greatly assist in the diagnosis and differential diagnosis of SS. This case not only enriches our understanding of SS and describes a rare site of origin, but also emphasizes the importance and challenges of achieving an accurate diagnosis. Immunohistochemical and molecular biological testing have important roles in the definitive diagnosis, highlighting the need for precise and innovative diagnostic and therapeutic approaches in SS.

Research progress on cuproptosis in cancer.

Cuproptosis is a recently discovered form of cell death that is mediated by copper (Cu) and is a non-apoptotic form of cell death related to oligomerization of lipoylated proteins and loss of Fe-S protein clusters. Since its discovery, cuproptosis has been extensively studied by researchers for its mechanism and potential applications in the treatment of cancer. Therefore, this article reviews the specific mechanism of cuproptosis currently studied, as well as its principles and strategies for use in anti-cancer treatment, with the aim of providing a reference for cuproptosis-based cancer therapy.

Effects of metronidazole on colorectal cancer occurrence and colorectal cancer liver metastases by regulating Fusobacterium nucleatum in mice.

OBJECTIVE: Colorectal cancer (CRC) represents a leading cause of cancer-related deaths. Metronidazole (MNZ) is exceedingly implicated in CRC. This study explored the roles of MNZ in mouse CRC occurrence and liver metastasis (CRLM). METHODS: Male BALB/c nude mice were subjected to CRC and CRLM modeling, orally administration with MNZ (1 g/L) 1 week before modeling, and disease activity index (DAI) evaluation. Fresh stool and anal swab samples were collected on the morning of the 28th day after modeling. The relative expression of Fusobacterium nucleatum (F. nucleatum) DNA was assessed by quantitative polymerase chain reaction. After euthanasia, tumor tissues and liver tissues were separated and the tumor volume and weight change were measured. The liver tissues were stained with hematoxylin-eosin to quantitatively analyze the metastatic liver nodules. Malignant tumor biomarker Ki67 protein levels in liver tissues/DNA from stool samples were detected by immunohistochemistry/high-throughput 16S rRNA gene sequencing. Bioinformatics analysis was performed on the raw sequence data to analyze microbial community richness (Chao1 index, ACE index) and microbial community diversity (Shannon index). RESULTS: The DAI and F. nucleatum DNA relative expression in feces and anal swabs of the CRC and CRLM groups were raised and repressed after MNZ intervention. MNZ repressed tumor occurrence and growth in mice to a certain extent, alleviated CRLM malignant degree (reduced liver metastases and Ki67-positive cell density/number), and suppressed CRC liver metastasis by regulating intestinal flora structure, which affected the intestinal characteristic flora of CRC and CRLM mice. CONCLUSION: MNZ suppressed CRC occurrence and CRLM in mice by regulating intestinal F. nucleatum.

Three specific gut bacteria in the occurrence and development of colorectal cancer: a concerted effort.

Colorectal cancer (CRC), which develops from the gradual evolution of tubular adenomas and serrated polyps in the colon and rectum, has a poor prognosis and a high mortality rate. In addition to genetics, lifestyle, and chronic diseases, intestinal integrity and microbiota (which facilitate digestion, metabolism, and immune regulation) could promote CRC development. For example, enterotoxigenic Bacteroides fragilis, genotoxic Escherichia coli (pks+ E. coli), and Fusobacterium nucleatum, members of the intestinal microbiota, are highly correlated in CRC. This review describes the roles and mechanisms of these three bacteria in CRC development. Their interaction during CRC initiation and progression has also been proposed. Our view is that in the precancerous stage of colorectal cancer, ETBF causes inflammation, leading to potential changes in intestinal ecology that may provide the basic conditions for pks+ E. coli colonization and induction of oncogenic mutations, when cancerous intestinal epithelial cells can further recruit F. nucleatum to colonise the lesion site and F. nucleatum may contribute to CRC advancement by primarily the development of cancer cells, stemization, and proliferation, which could create new and tailored preventive, screening and therapeutic interventions. However, there is the most dominant microbiota in each stage of CRC development, not neglecting the possibility that two or even all three bacteria could be engaged at any stage of the disease. The relationship between the associated gut microbiota and CRC development may provide important information for therapeutic strategies to assess the potential use of the associated gut microbiota in CRC studies, antibiotic therapy, and prevention strategies.

Small bowel intussusception caused by a serrated adenoma: a case report.

The case was a 17-year-old young woman with a one-year history of recurrent abdominal pain and discomfort. B-scan ultrasonography identified intussusception and contrast-enhanced computed tomography of the pelvis revealed volvulus. A laparoscopic procedure was planned to identify the reason for the intussusception and obstruction. Intraoperatively, the intussusception was found to be caused by a cauliflower-shaped polypoid tumor measuring approximately 4 × 3 cm. Postoperative pathological examination identified the tumor to be a traditional serrated adenoma of the small intestine, which is rare and has atypical clinical manifestations. If unexplained abdominal pain or gastrointestinal bleeding occurs and an abdominal mass cannot be accurately located, laparoscopic or open surgery should be performed immediately. Early surgery is the most effective and reliable way of securing a prompt diagnosis and a favorable prognosis.

Combination of antibiotics, gastric lavage and nasojejunal feeding-an effective alternative for the management of acute phlegmonous gastritis: a case report.

BACKGROUND: Phlegmonous gastritis is a rare bacterial infection of the gastric wall, characterised by purulent inflammation of the gastric mucosa, submucosa and muscularis layers. Phlegmonous gastritis has a high mortality rate, even with correct diagnosis and antimicrobial therapy. CASE PRESENTATION: A 22-year-old man presented for acute epigastric pain associated with aqueous diarrhoea, vomiting and sustained fever. Abdominal computed tomography showed diffuse oedema and thickened gastric wall, increased number and size of abdominal lymph nodes and the absence of pneumoperitoneum. Fibregastroscopy revealed oedematous, ridged and thickened gastric mucosa with abundant purulent secretion, especially in the antrum, consistent with phlegmonous gastritis, which was confirmed by histological evaluation of gastric biopsies. Cultures of the tissue biopsies and purulent secretion were positive for Enterococcus cecorum. He was treated with sensitive antibiotics according to the antibiogram, and importantly, with continuous gastric lavage and individualised nutritional support therapy. He eventually recovered well and was discharged with no abdominal symptoms. CONCLUSIONS: Our case indicates that early diagnosis and immediate treatment are crucial to achieve positive outcomes. The combination of sensitive antibiotics, gastric lavage and early enteral nutrition via nasojejunal feeding might be an effective alternative for the comprehensive treatment of acute phlegmonous gastritis.

Low Doses of Nonylphenol Promote Growth of Colon Cancer Cells through Activation of ERK1/2 via G Protein‒Coupled Receptor 30.

PURPOSE: Nonylphenol (NP) is an endocrine disruptor found in products such as cleaners, plastics, and detergents. It exerts actions similar to endogenous 17ß-estradiol (E2) and is reported to influence various cancers. However, its role in colon cancer remains elusive. MATERIALS AND METHODS: Colon cancer cell lines COLO 205 and SW480 were employed in our study. The cells were treated with NP or E2 followed by measurement of apoptosis and proliferation using flow cytometry and MTT assays, respectively. G protein-coupled estrogen receptor 30 (GPR30) expression was visualized using immunofluorescence and Western blot. To investigate the underlying mechanism, the expression levels of GPR30, p-protein kinase A (PKA), c-myc, cyclin D1, and ERK1/2 were analyzed using Western blot. Meanwhile, the GPR30 antagonist G15 was utilized to validate the role of GPR30 in colon cancer progression. Finally, the effect of a GPR30 inhibitor on tumor growth was determined in vivo using tumor xenograft mouse models. RESULTS: NP facilitated the proliferation of colon cancer cells and induced apoptosis failure in vitro. Western blot revealed increased GPR30 expression levels in response to NP treatment. Cyclin D1, p-PKA, c-myc, and proliferating cell nuclear antigen, proteins that regulate the cell cycle, were all upregulated by NP, and NP-mediated ERK1/2 activation and subsequent cell proliferation were abrogated by the GPR30 inhibitor G15. Moreover, colon cancer mice that received G15 administration demonstrated impaired tumor growth in vivo. CONCLUSION: Low dose NP promotes the growth of colon tumors through GPR30-mediated activation of ERK1/2 signaling.

LncRNA BCAR4, targeting to miR-665/STAT3 signaling, maintains cancer stem cells stemness and promotes tumorigenicity in colorectal cancer.

BACKGROUND: Breast cancer anti-estrogen resistance 4 (BCAR4) is closely associated with colorectal cancer (CRC) initiation and propagation. However, the mechanisms underlying BCAR4 function in colon cancer remains largely unknown. In this study, we hypothesized that BCAR4 could regulate colon cancer stem/initiating cells (CSC) function and further facilitates the colon cancer progression. METHODS: qRT-PCR was used to examine the expression of BCAR4 and various CSC markers. FACS, acetaldehyde dehydrogenase (ALDH) activity and western blot assays were applicable to test the expression of CSC markers. CCK8, tumorsphere formation and transwell assays were adopted to examine the capacity of CRC cells proliferation, self-renewal and migration. Pull down assay was used to test the interaction between BCAR4 and miR-665. Luciferase reporter assay was used to examine the interaction of miR-665 and activators of transcription (STAT3). In vivo tumor xenograft study was used to verify the malignancy of CRC cells with inhibition of BCAR4. RESULTS: Breast cancer anti-estrogen resistance 4 was highly expressed in both CRC cells and stem/initiating cells. In addition, overexpression of BCAR4 facilitated the maintenance of ALDH positive cells (a type of cancer stem/initiating cells) stemness and promoted ALDH+ cells proliferation and migration. Inhibition of BCAR4 restricted ALDH+ cells proliferation and migration. We further proved that miR-665 was the target of BCAR4 and subsequently activated signal transducers and STAT3 signaling which is an important pathway in cancer stem cells self-renewal. CONCLUSIONS: Breast cancer anti-estrogen resistance 4 promotes the CRC cells stemness through targeting to miR-665/STAT3 signaling and identification of the BCAR4 in CRC stem cells provides a new insight into CRC diagnosis, treatment, prognosis and next-step translational investigations.

Nonylphenol promotes the proliferation of colorectal cancer COLO205 cells by upregulating the expression of protein kinase C ζ.

Previous studies have indicated the potential role of estrogen in the development and prognosis of colorectal cancer (CRC). Nonylpheno (NP) is an endocrine-disrupting chemical, which may influence the development of estrogen-dependent types of cancer. However, the molecular mechanism of NP in the development of CRCs remains unclear. In the present study, various concentrations of NP were used to treat COLO205 CRC cells, and the expression of protein kinase C ζ (PKCζ) was knocked down using PKCζ small interfering RNA. The effects of NP in various concentrations on the cell cycle and apoptosis of COLO205 cells were examined, and the change in the expression level of PKCζ was analyzed. The results indicated that NP may significantly induce proliferation of COLO205 CRC cells, and significantly reduce cell apoptosis. However, suppression of PKCζ expression may inhibit proliferation, while NP could reduce this inhibition. The results of a western blot analysis indicated that the expression level of cyclin D1 and E were significantly increased following NP treatment, and the expression of p27 was significantly decreased. The phosphorylation of PKCζ and extracellular-signal-regulated kinase (ERK)1/2 was significantly increased following NP treatment in a dose-dependent manner. Overall, NP induced human CRC COLO205 cell proliferation and inhibited the apoptotic rate of COLO205 cells by increasing the activity of PKCζ and ERK1/2.

Effect of nonylphenol on the regulation of cell growth in colorectal cancer cells.

Nonylphenol (NP) is a well-known endocrine-disrupting chemical (EDC), which can enhance the progression of cancer by functioning as an estrogen­like factor. In the present study, the effects of different concentrations of NP on COLO205 colorectal cancer (CRC) cells were examined. The results of flow cytometric analysis revealed that NP significantly decreased the proportion of cells in the G0/G1 phase in a dose­dependent manner, which was accompanied by a marginal increase in the proportions of cells in S and G2/M phases. NP did not induce apoptosis, whereas estradiol (E2) did induce apoptosis. To elucidate the mechanisms underlying the action of NP on COLO205 cells, the transcriptional levels of extracellular signal­regulated kinase (ERK)1, ERK2 and phosphoinositide 3­kinase (PI3K) were assessed using reverse transcription­quantitative polymerase chain reaction analysis. The expressions levels of ERK1, ERK2 and PI3K were increased by treatment with NP in a dose­dependent manner. On examining protein levels, the expression of PI3K p38 was increased by NP and E2, and the expression of ERK1/2 was increased by NP. The phosphorylation of the ERK protein was significantly increased by treatment with NP at a high concentration (10­4 M; P<0.01), but significantly decreased by E2 (P<0.01). Two key proteins in the transforming growth factor (TGF)ß pathway (c­Fos and SnoN) were selected for analysis using western blot analysis in the COLO205 cells treated with NP and E2. The expression levels of c­Fos and SnoN were significantly increased by treatment with E2 (10­7 M; P<0.01) and NP (10­7­10­4 M; P<0.01). Taken together, these results indicated that NP affected the development of CRC via the ERK signaling pathway and TGFß pathway.

LPS-induced epithelial-mesenchymal transition of intrahepatic biliary epithelial cells.

BACKGROUND: Recent studies have revealed that the epithelial-mesenchymal transition (EMT) of bile duct epithelial cells is engaged in hepatic fibrogenesis. However, the association between etiological factors of liver disease such as virus or bacterial infection and EMT remains to be investigated. The present study focuses on the inductive role of endotoxin, the main component of the cell wall's ectoblast of gram-negative bacteria, in the EMT of human intrahepatic biliary epithelial cells (HIBEpiCs). METHODS: The expressions of E-cadherin, S100A4, α-SMA, TGF-ß1, and Smad2/3 in HIBEpiCs cultured with or without lipopolysaccharide LPS, were detected by real-time PCR and Western blotting. We blocked the expression of TGF-ß1 using paclitaxel and knocked down Smad2/3 by siRNA to explore the role of TGF-ß1/Smad2/3 pathway in the EMT of HIBEpiCs. RESULTS: Resting HIBEpiCs showed epithelioid cobblestone morphology, and underwent a phenotypic change to produce bipolar cells with a fibroblastic morphology when co-cultured with LPS. After LPS stimulation and the up-regulation of mRNA and protein expression of TGF-ß1 and Smad2/Smad3, the mRNA and protein expression of mesenchymal markers (S100A and α-SMA) increased significantly. Paclitaxel inhibited the mRNA and protein expression of TGF-ß1 in vitro. Knock-down of Smad2/3 by siRNA led to up-regulation of epithelial markers E-cadherin and down-regulation of S100A and α-SMA, indicating a reversal of the EMT. CONCLUSIONS: LPS can induce the expression of TGF-ß1 and a subsequent EMT in HIBEpiCs, and the inhibition of TGF-ß1 or Smad 2/3 could reverse this EMT, suggesting that LPS may play a potential role in the EMT of HIBEpiCs.

Epithelial-mesenchymal transitions of bile duct epithelial cells in primary hepatolithiasis.

The purpose of this study was to explore the role of epithelial-mesenchymal transition in the pathogenesis of hepatolithiasis. Thirty-one patients with primary hepatolithiasis were enrolled in this study. Expressions of E-cadherin, alpha-catenin, alpha-SMA, vimentin, S100A4, TGF-beta1 and P-smad2/3 in hepatolithiasis bile duct epithelial cells were examined by immunohistochemistry staining. The results showed that the expressions of the epithelial markers E-cadherin and alpha-catenin were frequently lost in hepatolithiasis (32.3% and 25.9% of cases, respectively), while the mesenchymal markers vimentin, alpha-SMA and S100A4 were found to be present in hepatolithiasis (35.5%, 29.0%, and 32.3% of cases, respectively). The increased mesenchymal marker expression was correlated with decreased epithelial marker expression. The expressions of TGF-beta1 and P-smad2/3 in hepatolithiasis were correlated with the expression of S100A4. These data indicate that TGF-beta1-mediated epithelial-mesenchymal transition might be involved in the formation of hepatolithiasis.