Cancer stem cell markers CD44v9+/CD133- are associated with low apoptosis in both sporadic and ulcerative colitis-associated colorectal cancers

xlomafota13 shared this article with you from Inoreader Cancer stem cell markers CD44v9+/CD133- are associated with low apoptosis in both sporadic and ulcerative colitis-associated colorectal cancers Via Cellular and Molecular Biology Histol Histopathol. 2022 Feb 28:18445. doi: 10.14670/HH-18-445. Online ahead of print. ABSTRACT OBJECTIVE: To elucidate tumor cell behavior associated with cancer stem cell (CSC) marker expression, the expression of CD133, CD44v9, and ALDH1A1, which are considered markers of CSCs, was examined in sporadic and ulcerative colitis (UC)-associated colorectal tumors. METHODS: A total of 23 cases of sporadic colorectal cancer and 44 cases of adenoma were collected. Additionally, 22 cancer lesions and 38 dysplasia lesions were selected from 28 colectomy cases of UC with neoplastic lesions. Lesions were examined by immunohistochemistry using primary antibodies against CD133, CD44v9, ALDH1A1, Ki-67, cleaved-Caspase 3, and p53. RESULTS: CD133, CD44v9, and ALDH1A1 showed higher expression in both sporadic and UC-associated tumors than in the normal mucosa. ALDH1A1 expression in sporadic cancer was higher in the right colon than in the left colon (p=0.0089). ALDH1A1 expression in UC-associated cancer was higher in those with longer disease duration than in those with shorter disease duration (p=0.019). The CD44v9+/CD133- region had fewer cleaved-Caspase 3 positive cells in both sporadic and UC-associated cancers. In sporadic cancer, CD133+/ALDH1A1+ regions had fewer apoptotic cells than CD133+/ALDH1A1- regions, while CD133+/ALDH1A1- regions were less proliferative than CD133+/ALDH1A1+ regions in UC-associated cancer. CONCLUSION: CD44+/CD133- regions were commonly associated with low apoptosis in sporadic and UC-associated cancers; thus, these were considered target areas for CSCs. Additionally, the combination of markers comprising CSCs may differ between sporadic and UC-associated cancers. PMID:35224715 | DOI:10.14670/HH-18-445 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Ventriculoperitoneal Shunt Alone for Cerebrospinal Fluid Rhinorrhea With Neuroendocrine Alterations in Idiopathic Intracranial Hypertension: A Case Report and Literature Review

xlomafota13 shared this article with you from Inoreader Ventriculoperitoneal Shunt Alone for Cerebrospinal Fluid Rhinorrhea With Neuroendocrine Alterations in Idiopathic Intracranial Hypertension: A Case Report and Literature Review Via leak of cerebrospinal fluid Front Neurol. 2022 Feb 10;13:809224. doi: 10.3389/fneur.2022.809224. eCollection 2022. ABSTRACT Spontaneous skull base cerebrospinal fluid (CSF) leaks due to idiopathic intracranial hypertension (IIH) are a rare entity. Patients often present with CSF rhinorrhea, recurrent meningitis, chronic headache, and visual defects, while few patients have been reported to present with neuroendocrine alterations. Endonasal endoscopic repair is the first-line treatment for these leaks at present. However, the relatively high risk of recurrence remains the main cause of reoperation because of elevated intracranial pressure (ICP) after endoscopic surgery and absence of postoperative ICP management. A shunting procedure may stop CSF leakage or relieve symptoms in complex cases, and this is presently well-known as the last-line therapy for CSF liquorrhea. We describe a 29-year-old woman with spontaneous CSF rhinorrhea and neuroendocrine alterations due to II H, and with no previous history of trauma, tumor, or nasal surgery. The bone defect in the skull base became implicated when the site of the leak was detected by cranial magnetic resonance imaging and computed tomography (CT). The patient was successfully managed via ventriculoperitoneal shunt (VPS) alone without endoscopic repair, and neuroendocrine alterations resolved after the shunting procedure. PMID:35222246 | PMC:PMC8866819 | DOI:10.3389/fneur.2022.809224 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Impact of metabolic disorders on endometrial receptivity in patients with polycystic ovary syndrome

xlomafota13 shared this article with you from Inoreader Impact of metabolic disorders on endometrial receptivity in patients with polycystic ovary syndrome Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):221. doi: 10.3892/etm.2022.11145. Epub 2022 Jan 14. ABSTRACT The present study investigated the expression of endometrial receptivity-related molecules in patients with polycystic ovary syndrome (PCOS) and different androgen status, insulin resistance (IR) levels, and body mass indexes (BMI) to identify the mechanism underlying their effects on pregnancy outcomes. The present study recruited 43 participants from November 2020 to January 2021, which were classified into five groups: i) Hyperandrogenemia (HA) combined with impaired glucose tolerance group (n=8); ii) HA combined with diabetes mellitus group (n=8); iii) HA combined with non-IR (NIR) group (n=10); iv) non-HA (NHA) androgen combined with IR group (n=8); and v) NHA combined with NIR group (n=9). In addition, according to their BMIs, patients were sub-grouped into lean/normal (n=27), overweight (n=8) or obese (n=8) groups. The mRNA expression level s of endometrial receptivity-related molecules were detected using reverse transcription-quantitative PCR. In addition, flow cytometry was used to determine the phenotype and percentage of uterine natural killer cells (uNK). According to the results, patients with PCOS and IR status, HA and obesity (BMI ≥24 kg/m2) demonstrated significantly decreased mRNA expression levels of adiponectin, adiponectin receptor (AdipoR)1, AdipoR2, adapter protein containing PH domain, PTB domain and leucine zipper motif 1, estrogen receptor (ER) α, ERβ, progesterone receptor (PR), IL-15, integrin β3 avβ3, and insulin-like growth factor binding protein-1, but increased mRNA expression levels of IL-6 and IL-8 compared with NHA + NIR group or lean/normal group, respectively. In addition, obese patients with PCOS demonstrated increased mRNA expression levels of PR compared with overweight patients. This suggested that insulin resistant status, HA, and obesity could alter the endometrial r eceptivity of patients with PCOS, which may explain poorer embryo implantation and pregnancy outcomes in clinics. PMID:35222698 | PMC:PMC8812101 | DOI:10.3892/etm.2022.11145 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

LACTB suppresses carcinogenesis in lung cancer and regulates the EMT pathway

xlomafota13 shared this article with you from Inoreader LACTB suppresses carcinogenesis in lung cancer and regulates the EMT pathway Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):247. doi: 10.3892/etm.2022.11172. Epub 2022 Jan 28. ABSTRACT Lung cancer causes thousands of deaths worldwide every year, and present therapeutics show little benefit for advanced-stage patients. Researchers do not know why and how lung cancer begins. Lactamase β (LACTB) is a tumor-suppressor in some cancers. However, its role in lung cancer is unknown. By analyzing the TCGA database and Kaplan-Meier Plotter database, LACTB was found to be downregulated in lung cancer tissues but the methylation level was increased. Patients with high LACTB expression exhibited improved survival. Then, in vitro assays demonstrated that LACTB overexpression inhibited cell migration and invasion, and induced apoptosis in H1299 and H1975 cells. Knockdown of LACTB caused the reverse effects. Moreover, a much higher apoptotic rate and more potent inhibitory effects on H1299 and H1975 cells wer e obtained when LACTB was combined with docetaxel. In addition, members of the epithelial-mesenchymal transition (EMT) signaling pathway were assessed using western blot analysis. The expression of E-cadherin was decreased while levels of N-cadherin and vimentin were increased after knockdown of LACTB in lung cancer cells. By contrast, overexpression of LACTB increased the level of E-cadherin but decreased N-cadherin and vimentin. Therefore, LACTB is a tumor suppressor in lung cancer that inhibits cell migration and invasion and induces cell apoptosis. Meanwhile, LACTB was found to strengthen the anticancer role of docetaxel and to suppress the EMT pathway in lung cancer. PMID:35222724 | PMC:PMC8815028 | DOI:10.3892/etm.2022.11172 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Estrogen downregulates TAK1 expression in human fibroblast-like synoviocytes and in a rheumatoid arthritis model

xlomafota13 shared this article with you from Inoreader Erratum: Estrogen downregulates TAK1 expression in human fibroblast-like synoviocytes and in a rheumatoid arthritis model Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):225. doi: 10.3892/etm.2022.11149. Epub 2022 Jan 17. ABSTRACT [This corrects the article DOI: 10.3892/etm.2020.8848.]. PMID:35222702 | PMC:PMC8812110 | DOI:10.3892/etm.2022.11149 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Long non-coding RNA ATB is associated with metastases and promotes cell invasion in colorectal cancer via sponging miR-141-3p

xlomafota13 shared this article with you from Inoreader Erratum: Long non-coding RNA ATB is associated with metastases and promotes cell invasion in colorectal cancer via sponging miR-141-3p Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):238. doi: 10.3892/etm.2022.11163. Epub 2022 Jan 24. ABSTRACT [This corrects the article DOI: 10.3892/etm.2020.9391.]. PMID:35222715 | PMC:PMC8815047 | DOI:10.3892/etm.2022.11163 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Metformin reduces chondrocyte pyroptosis in an osteoarthritis mouse model by inhibiting NLRP3 inflammasome activation

xlomafota13 shared this article with you from Inoreader Metformin reduces chondrocyte pyroptosis in an osteoarthritis mouse model by inhibiting NLRP3 inflammasome activation Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):222. doi: 10.3892/etm.2022.11146. Epub 2022 Jan 17. ABSTRACT Osteoarthritis (OA) is an age-related degenerative disease, and its incidence is increasing with the ageing of the population. Metformin, as the first-line medication for the treatment of diabetes, has received increasing attention for its role in OA. The purpose of the present study was to confirm the therapeutic effect of metformin in a mouse model of OA and to determine the mechanism underlying the resultant delay in OA progression. The right knees of 8-week-old C57BL/6 male mice were subjected to destabilization of the medial meniscus (DMM). Metformin (200 mg/kg) was then administered daily for 4 or 8 weeks. Safranin O-fast green staining, H&E staining and micro-CT were used to analyse the structure and morphological changes. Immunohistochemical staining was used to detect type II collagen (Col II), matrix metalloproteinase 13 (MMP-13), NO D-like receptor protein 3 (NLRP3), caspase-1, gasdermin D (GSDMD) and IL-1β protein expression. Reverse transcription-quantitative PCR was used to detect the mRNA expression of NLRP3, caspase-1, GSDMD and IL-1β. Histomorphological staining showed that metformin delayed the progression of OA in the DMM model. With respect to cartilage, metformin decreased the Osteoarthritis Research Society International score, increased the thickness of hyaline cartilage and decreased the thickness of calcified cartilage. Regarding the mechanism, in cartilage, metformin increased the expression of Col II and decreased the expression of MMP-13, NLRP3, caspase-1, GSDMD and IL-1β. In addition, in subchondral bone, metformin inhibited osteophyte formation, increased the bone volume fraction (%) and the bone mineral density (g/cm3), decreased the trabecular separation (mm) in early stage of osteoarthritis (4 weeks) but the opposite in an advanced stage of osteoarthritis (8 weeks). Overall, metformin inhibited the activation of NLRP3 inflammasome, decreased cartilage degradation, reversed subchondral bone remodelling and inhibited chondrocyte pyroptosis. PMID:35222699 | PMC:PMC8812147 | DOI:10.3892/etm.2022.11146 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.