Expression of STAT3 and vasculogenic mimicry in gallbladder carcinoma promotes invasion and metastasis

xlomafota13 shared this article with you from Inoreader Expression of STAT3 and vasculogenic mimicry in gallbladder carcinoma promotes invasion and metastasis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):738. doi: 10.3892/etm.2021.10170. Epub 2021 May 9. ABSTRACT Surgical treatment of gallbladder carcinoma remains challenging, while targeted therapy has been demonstrated to have potential. In the present study, the effect of signal transducer and activator of transcription 3 (STAT3) expression and vasculogenic mimicry (VM) on the occurrence and development of gallbladder carcinoma was evaluated. A total of 72 patients with gallbladder carcinoma and 10 patients with chronic cholecystitis were examined. Immunohistochemical staining was performed to determine the positive expression rates of STAT3. Periodic acid Schiff CD34 double staining was performed to detect VM in the gallbladder carcinoma group. STAT3 expression and VM in gallbladder carcinoma tissues was compared among patients with different clinical characteristics. In postoperative patients with gallbladder cancer, the relationship of the postoperati ve recurrence time with STAT3 expression and VM was assessed. STAT3 expression in gallbladder carcinoma tissue was significantly higher than that in cholecystitis tissue (P<0.05). STAT3 expression levels and VM were positively correlated in gallbladder carcinoma tissue. STAT3 protein expression in gallbladder carcinoma tissues differed significantly among patients with different degrees of differentiation and clinical stages (P<0.05). Among the 51 patients who completed the 3-year follow-up, the mean time to relapse was 17.353 and 35.647 months in those with high and low STAT3 expression, respectively, with significant differences (P<0.05). The VM structure was detected in 47 cases (92.15%) and not detected in four cases (7.84%), which exhibited no immediate recurrence after surgery, and the difference in the mean postoperative recurrence time was significant (22.38 vs. 36.00 months, respectively; P<0.05). In gallbladder carcinoma tissues, a lower degree of differentiati on, higher malignancy degree and higher clinical stage were associated with higher expression of STAT3 and VM. Thus, STAT3 may promote VM formation in the process of tumor occurrence, development and metastasis. Therefore, STAT3 as a regulatory target, may inhibit the proliferation and invasion of tumor cells and block the development of VM, thereby representing a suitable target for antitumor angiogenesis therapy. PMID:34055055 | PMC:PMC8138270 | DOI:10.3892/etm.2021.10170 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Tumoral markers in bladder cancer (Review)

xlomafota13 shared this article with you from Inoreader Tumoral markers in bladder cancer (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):773. doi: 10.3892/etm.2021.10205. Epub 2021 May 18. ABSTRACT Bladder tumors are frequently diagnosed urologic malignant diseases with an extremely high recurrence rate compared to other neoplastic tumors. Urothelial bladder carcinomas are mostly identified in their incipient form, as non-muscle invasive, but despite that, a third of them develop into aggressive recurrent disease. The diagnosis of bladder carcinoma at this moment is established using cytology and cystoscopy and is a great challenge for clinicians due to the lack of sensitivity. Urinary biomarkers could improve and enhance the diagnosis and screening techniques and determine a more accurate recurrence rate. However, bladder cancer is a heterogeneous disease and the existence of a single marker test with reduced cost is unlikely; thus, until then, the use of a panel of markers to obtain valuable information is inevitable even though suboptimal for use. To improve this deadlock, new biomarker panels should be identified and prepared to equalize the cost-efficiency balance. The present paper is a literature review concerning the most commonly used tumor markers in urinary bladder cancer as well as the most commonly encountered genetic modifications in such patients. PMID:34055072 | PMC:PMC8145526 | DOI:10.3892/etm.2021.10205 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Hirsutanol A inhibits T-acute lymphocytic leukemia Jurkat cell viability through cell cycle arrest and p53-dependent induction of apoptosis

xlomafota13 shared this article with you from Inoreader Hirsutanol A inhibits T-acute lymphocytic leukemia Jurkat cell viability through cell cycle arrest and p53-dependent induction of apoptosis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):741. doi: 10.3892/etm.2021.10173. Epub 2021 May 11. ABSTRACT Acute lymphocytic leukemia (ALL) is a type of childhood leukemia with the highest incidence; T-acute lymphocytic leukemia (T-ALL) is far more difficult to treat than B-acute lymphocytic leukemia (B-ALL) and has a poor long-term prognosis. Therefore, there is an urgent requirement to develop effective drugs for the treatment of T-ALL. Hirsutanol A is a natural sesquiterpenoid compound. The aim of the present study was to evaluate the in vitro anticancer activity of hirsutanol A against T-acute lymphocytic leukemia Jurkat cells and investigate the mechanism of action. A Cell Counting Kit-8 assay demonstrated that hirsutanol A inhibited the viability of Jurkat cells in a dose- and time-dependent manner. In addition, hirsutanol A induced cell cycle arrest at the G2 phase as determined via flow cytometry. Furthermore, Hoechst staining , Annexin V-FITC/propidium iodide double staining, mitochondrial membrane potential detection using JC-1 and western blot analysis of apoptotic proteins indicated that the inhibitory effect of hirsutanol A on Jurkat cells was associated with the induction of apoptosis. Of note, hirsutanol A induced the expression of the tumor suppressor p53, whereas simultaneous treatment with pifithrin-α, an inhibitor of p53, significantly reduced Jurkat cell apoptosis induced by hirsutanol A. In summary, the present study suggested that hirsutanol A inhibited Jurkat cell viability through induction of cell cycle arrest and p53-dependent initiation of apoptosis, thus hirsutanol may serve as a promising compound for the treatment of T-ALL. PMID:34055057 | PMC:PMC8138276 | DOI:10.3892/etm.2021.10173 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

B7 homolog 6 promotes the progression of cervical cancer

xlomafota13 shared this article with you from Inoreader B7 homolog 6 promotes the progression of cervical cancer Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):774. doi: 10.3892/etm.2021.10206. Epub 2021 May 18. ABSTRACT B7 homolog 6 (B7-H6) was recently discovered to act as a co-stimulatory molecule. In particular, the expression of B7-H6 has been found to play an important biological role in several types of tumors. The aim of the present study was to determine the role of B7-H6 in cervical cancer. Immunohistochemistry was used to analyze the expression levels of B7-H6 in cervical precancerous and cancerous tissues. Furthermore, the expression of B7-H6 was knocked down in HeLa cells using short hairpin RNA and the effects of B7-H6 on HeLa cell proliferation, migration and invasion were determined using Cell Counting Kit-8, colony formation, wound healing and Transwell invasion assays, respectively. In addition, flow cytometry was used to analyze the levels of cell apoptosis and the cell cycle distribution. The results of the immunohistochemical staining revealed that the expression levels of B7-H6 were upregulated in cervical lesions. Furthermore, the expression levels of B7-H6 were positively associated with the clinical stage of the cervical lesions. B7-H6 knockdown suppressed the invasive, migratory and proliferative abilities of HeLa cells, and promoted G1 cell cycle arrest and apoptosis. In conclusion, the findings of the present study suggested that B7-H6 may serve as a novel oncogene and may hold promise as a potential therapeutic target for cervical cancer. PMID:34055073 | PMC:PMC8145428 | DOI:10.3892/etm.2021.10206 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Rosiglitazone alleviates lipopolysaccharide-induced inflammation in RAW264.7 cells via inhibition of NF-κB and in a PPARγ-dependent manner

xlomafota13 shared this article with you from Inoreader Rosiglitazone alleviates lipopolysaccharide-induced inflammation in RAW264.7 cells via inhibition of NF-κB and in a PPARγ-dependent manner Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):743. doi: 10.3892/etm.2021.10175. Epub 2021 May 11. ABSTRACT Rosiglitazone is a synthetic peroxisome proliferator-activated receptor (PPAR)γ agonist widely used for the treatment of type 2 diabetes. Recent studies have demonstrated that rosiglitazone displays anti-inflammatory effects. The present study aimed to investigate whether rosiglitazone alleviates decreases in RAW264.7 cell viability resulting from lipopolysaccharide (LPS)-induced inflammation, as well as exploring the underlying mechanism. A macrophage inflammatory injury model was established by treating RAW264.7 cells with 100 ng/ml LPS. Cells were divided into LPS and rosiglitazone groups with different concentrations. Cell viability was assessed by performing an MTT assay. The expression of inflammatory cytokines was detected by conducting enzyme-linked immunosorbent assays and reverse transcription-quantitative PCR. Nitric oxidesecretion was assessed using the Griess reagent system. The expression levels of key nuclear factor-κB pathway-associated proteins were detected via western blotting. Rosiglitazone alleviated LPS-induced decrease in RAW264.7 cell viability and inhibited inflammatory cytokine expression in a concentration-dependent manner. Rosiglitazone significantly inhibited LPS-induced upregulation of p65 phosphorylation levels and downregulated IκBα expression levels. However, rosiglitazone-mediated inhibitory effects were reversed by PPARγ knockdown. The results of the present study demonstrated that rosiglitazone significantly inhibited LPS-induced inflammatory responses in RAW264.7 macrophage cells, which was dependent on PPARγ activation and NF-κB suppression. PMID:34055059 | PMC:PMC8138265 | DOI:10.3892/etm.2021.10175 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Diabetic neuropathic pain induced by streptozotocin alters the expression profile of non-coding RNAs in the spinal cord of mice as determined by sequencing analysis

xlomafota13 shared this article with you from Inoreader Diabetic neuropathic pain induced by streptozotocin alters the expression profile of non-coding RNAs in the spinal cord of mice as determined by sequencing analysis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):775. doi: 10.3892/etm.2021.10207. Epub 2021 May 18. ABSTRACT Diabetic neuropathic pain (DNP) is one of the most serious complications of diabetes. Patients with DNP always exhibit spontaneous and stimulus-evoked pain. However, the pathogenesis of DNP remains to be fully elucidated. Non-coding RNAs (ncRNAs) serve important roles in several cellular processes and dysregulated expression may result in the development of several diseases, including DNP. Although ncRNAs have been suggested to be involved in the pathogenesis of DNP, their precise roles remain to be determined. In the present study, sequencing analysis was used to investigate the expression patterns of coding genes, microRNAs (miRNAs), long ncRNAs (lncRNAs) and circular RNAs (circRNAs) in the spinal cord of mice with streptozotocin (STZ)-induced DNP. A total of 30 mRNAs, 148 miRNAs, 9 lncRNAs and 135 circRNAs exhibited significantly dysregulated expression 42 days after STZ injection. Functional enrichment analysis indicated that protein digestion and absorption pathways were the most significantly affected pathways of the differentially expressed (DE) mRNAs. The Rap1 signaling pathway, human T-lymphotropic virus-I infection and the MAPK signaling pathway were the three most significant pathways of the DE miRNAs. A total of 2,118 distinct circRNAs were identified and the length of the majority of the circRNAs was <1,000 nucleotides (nt) (1,552 circRNAs were >1,000 nt) with a median length of 620 nt. In the present study, the expression characteristics of coding genes, miRNAs, lncRNAs and circRNAs in DNP mice were determined; it paves the road for further studies on the mechanisms associated with DNP and potentially facilitates the discovery of novel ncRNAs for therapeutic targeting in the management of DNP. PMID:34055074 | PMC:PMC8145263 | DOI:10.3892/etm.2021.10207 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Nephrogenic diabetes insipidus in children (Review)

xlomafota13 shared this article with you from Inoreader Nephrogenic diabetes insipidus in children (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):746. doi: 10.3892/etm.2021.10178. Epub 2021 May 11. ABSTRACT Nephrogenic diabetes insipidus (NDI) is characterized by impaired urinary concentrating ability, despite normal or elevated plasma concentrations of the antidiuretic hormone, arginine vasopressin (AVP). NDI can be inherited or acquired. NDI can result from genetic abnormalities, such as mutations in the vasopressin V2 receptor (AVPR2) or the aquaporin-2 (AQP2) water channel, or acquired causes, such as chronic lithium therapy. Congenital NDI is a rare condition. Mutations in AVPR2 are responsible for approximately 90% of patients with congenital NDI, and they have an X-linked pattern of inheritance. In approximately 10% of patients, congenital NDI has an autosomal recessive or dominant pattern of inheritance with mutations in the AQP2 gene. In 2% of cases, the genetic cause is unknown. The main symptoms at presentation include growth retardation, vomiting or feeding concerns, polyuria plus polydipsia, and dehydration. Without treatment, most patients fail to grow normally, and present with associated constipation, urological complication, megacystis, trabeculated bladder, hydroureter, hydronephrosis, and mental retardation. Treatment of NDI consist of sufficient water intake, low-sodium diet, diuretic thiazide, sometimes in combination with a cyclooxygenase (COX) inhibitor (indomethacin) or nonsteroidal anti-inflammatory drugs (NSAIDs), or hydrochlorothiazide in combination with amiloride. Some authors note a generally favorable long-term outcome and an apparent loss of efficacy of medical treatment during school age. PMID:34055061 | PMC:PMC8138272 | DOI:10.3892/etm.2021.10178 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

CLCA2 suppresses the proliferation, migration and invasion of cervical cancer

xlomafota13 shared this article with you from Inoreader CLCA2 suppresses the proliferation, migration and invasion of cervical cancer Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):776. doi: 10.3892/etm.2021.10208. Epub 2021 May 18. ABSTRACT Ca2+-activated Cl- channel A2 (CLCA2), a tumor suppressor, is associated with the development of several cancers. However, little is known about CLCA2 in human cervical cancer. Therefore, the aim of the present study was to investigate the effects of CLCA2 on cervical cancer. Reverse transcription-quantitative (RT-q)PCR was used to examine the mRNA expression levels of CLCA2 in eight pairs of cervical cancer tissues. Immunohistochemistry was used to investigate CLCA2 protein expression in 144 archived cervical cancer specimens. The association of the CLCA2 with clinicopathological parameters was statistically evaluated. Cell proliferation and invasion capability were examined by MTT and Transwell assays, respectively. RT-qPCR analysis revealed that CLCA2 expression was decreased in cervical cancer compared with that in adjace nt normal tissues. The expression levels of CLCA2 in patients were correlated with tumor stage (P=0.028), tumor size (P=0.009), and human papillomavirus (HPV) infection status (P=0.041). In addition, CLCA2 upregulation was associated with longer overall and recurrence-free survival time after surgery (P=0.016 and P=0.009, respectively). Multivariate Cox regression analysis demonstrated that CLCA2 expression had a predictive value for overall survival of patients with cervical cancer (P=0.017 and P=0.025, respectively). Knockdown of CLCA2 by small interfering RNA suppressed tumor cell proliferation and migration. Mechanistically, CLCA2 was involved in Wnt/β-catenin signaling. In conclusion, the results of the present study demonstrated that CLCA2 suppressed the proliferation, migration and invasion of cervical cancer cells, and that CLCA2 may be a potential therapeutic target of cervical cancer. PMID:34055075 | PMC:PMC8145432 | DOI:10.3892/etm.2021.10208 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Antibiotic resistance patterns of urinary tract pathogens in children from Central Romania

xlomafota13 shared this article with you from Inoreader Antibiotic resistance patterns of urinary tract pathogens in children from Central Romania Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):748. doi: 10.3892/etm.2021.10180. Epub 2021 May 12. ABSTRACT One of the most frequent bacterial infections in children are urinary tract infections (UTIs). In recent years, an increasing incidence of UTIs caused by resistant bacterial strains has been observed, especially with extended-spectrum β-lactamase-producing Enterobacteriaceae that represent about 15% of UTIs. A retrospective study was performed comprising 331 pediatric cases with UTI. Our study aimed to detect the resistance of the uropathogens to common drugs used in UTI treatment. High resistance rates have been recorded for ampicillin, amoxicillin, trimethoprim/sulfamethoxazole (TMP/SMX), cefuroxime, and ciprofloxacin, among E. coli and Klebsiella. The multidrug-resistance (MDR) rate was detected in one-third of the uropathogens, among which more than half were isolated in patients with urinary tract abnormalities. Our study highl ighted that nitrofurantoin, ceftriaxone, amikacin and carbapenem may be used for the empirical treatment for febrile or complicated UTI in children. This is the first comprehensive study that evaluates antibiotic resistance in UTIs in children, and their association with urinary tract abnormalities in Romania. As a result of this research, the protocol for initial empiric treatment of infants with febrile or complicated UTI should be modified considering a detailed and ongoing monitoring of local sensitivity of uropathogens to antimicrobial agents. PMID:34055063 | PMC:PMC8138273 | DOI:10.3892/etm.2021.10180 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Analysis of the effects of prepared porcelain veneers and unprepared porcelain veneers on gingival crevicular flora based on high-throughput sequencing

xlomafota13 shared this article with you from Inoreader Analysis of the effects of prepared porcelain veneers and unprepared porcelain veneers on gingival crevicular flora based on high-throughput sequencing Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):777. doi: 10.3892/etm.2021.10209. Epub 2021 May 18. ABSTRACT The effect of tooth preparation on the gingival crevicular flora of abutment teeth during porcelain veneer treatment is not clear. The purpose of the present study was to analyze the difference between prepared porcelain veneers and unprepared porcelain veneers on gingival crevicular flora. High-throughput sequencing was used in the present study. A total of 20 patients (40 anterior teeth) with veneer restoration of anterior teeth were enrolled. They were divided into two groups: The prepared porcelain veneer group (group P, 11 cases, 19 anterior teeth) and unprepared porcelain veneer group (group U, 9 cases, 21 anterior teeth). After 2 years of follow-up, the restoration and healthy natural gingival crevicular fluid were collected to extract bacterial DNA. 16S ribosomal DNA high-throughput sequencing technique was used to compare the diversity of gingival sulcus flora structure between the prepared porcelain veneer and unprepared porcelain veneer groups. In addition, a healthy control group (group H) was also used for comparison. The Shannon index of the group U was lower than that of group H and group P. The abundance of Proteus in group U was higher than that in group H and group P at the phylum level (P<0.05). At the genus level, the abundance of Porphyromonas, Prevotella and Actinomycetes in group U was significantly higher than that in group H and group P (P<0.05). Compared with the group P, the bacterial diversity of the group U was lower, and the proportion of gingival sulcus pathogenic bacteria was higher. The unprepared porcelain veneer had a certain adverse effect on the periodontal tissue. PMID:34055076 | PMC:PMC8145799 | DOI:10.3892/etm.2021.10209 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.