The sialic acid-binding immunoglobulin-type lectin Siglec-15 is a promising target to cancer immunotherapy in several tumor types. The present study aimed to investigate Siglec-15 expression in gastric cancer (GC) patient tissue and to evaluate its clinical value. Siglec-15 expression was evaluated by immunohistochemistry with 71 patients. Siglec-15 staining was observed in tumor cells of 53 (74.64%) patients, with significant association with histologic classification and angiolymphatic invasion (p<0.05). Immunohistochemistry analysis also detected Siglec-15 in tumor-associated stroma cells (macrophages/myeloid cells). There was no significant association with outcomes parameters. Siglec-15 expression in well differentiated histological GC tissues and in the tumor microenvironment are potential targets to be further investigated as a novel prognostic factor for GC.
The frontal sinuses are cranial areas of clinical, forensic and pathology importance whose development mechanisms are still poorly defined. Nasal airflow and brain development are two of the main theories. Current analysis debates whether they are the real determinants of frontal sinuses growth, which may be proved by the skull's morphometric analysis. Four groups of measures related to the external cranial architecture, the pyriform aperture, orbital cavities and frontal sinuses were defined. Thirty-three skulls of individuals, mean age 68 years, from the Laboratory of Anatomy of the Academic Centre of Victoria-UFPE-Brazil, were used. Statistical analysis showed total agenesis of the frontal sinus in 18.2% of the skulls. There was significant correlation between the development of the right frontal sinus and the pyriform aperture, and between the left frontal sinus and two cranial measurements (p ≤ 0.05). Significant differences between mean of pyriform aperture areas of the skulls with or without sinuses were also reported (p ≤ 0.01). Results supported the fact that there was a modulation activity by nasal aeration and brain formation in the development of frontal sinuses.
Pancreatic ductal adenocarcinoma is one of the most aggressive tumors with a microenvironment marked by hypoxia and starvation. Galectin-3 has been evaluated in solid tumors and seems to present both pro/anti-tumor effects. So, this study aims to characterize the expression of Galectin-3 from pancreatic tumor cells and analyze its influence for cell survive and motility in mimetic microenvironment. For this, cell cycle and cell death were accessed through flow cytometry. Characterization of inside and outside Galectin-3 was performed through Real-Time Quantitative Reverse Transcription PCR (qRT-PCR), immunofluorescence, Western blot, and ELISA. Consequences of Galectin-3 extracellular inhibition were investigated using cell death and scratch assays. PANC-1 showed increased Galectin-3 mRNA expression when cultivated in hypoxia for 24 and 48 h. After 24 h in simultaneously hypoxic/deprived incubation, PANC-1 shows increased Galectin-3 protein and secreted levels. For Mia PaCa-2, cultivation in deprivation was determinant for the increasing in Galectin-3 mRNA expression. When cultivated in simultaneously hypoxic/deprived condition, Mia PaCa-2 also presented increasing for the Galectin-3 secreted levels. Treatment of PANC-1 cells with lactose increased the death rate when cells were incubated simultaneously hypoxic/deprived condition. Therefore, it is possible to conclude that the microenvironmental conditions modulate the Galectin-3 expression on the transcriptional and translational levels for pancreatic cancer cells.
One of the greatest challenges of cancer therapeutics nowadays is to find selective targets successfully. Prostate apoptosis response-4 (Par-4) is a selective tumor suppressor protein with an interesting therapeutic potential due to its specificity on inducing apoptosis in cancer cells. Par-4 activity and levels can be downregulated in several tumors and cancer cell types, indicating poor prognosis and treatment resistance. Efforts to increase Par-4 expression levels have been studied, including its use as a therapeutic protein by transfection with adenoviral vectors or plasmids. However, gene therapy is very complex and still presents many hurdles to be overcome. We decided to review molecules and drugs with the capacity to upregulate Par-4 and, thereby, be an alternative to reach this druggable target. In addition, Par-4 localization and function are reviewed in some cancers, clarifying how it can be used as a therapeutic target.
Hypoxic areas in solid tumors are often associated with poor prognosis and resistance to chemotherapy. The aim of the study was to analyze the expression of galectin-1 (Gal-1), galectin-3 (Gal-3), sialic acid and b1-6 branched glycan structures in hypoxic environment of invasive ductal carcinoma (IDC) of the breast. We performed lectin histochemistry with phytohemagglutinin-L (L-PHA) and Sambucus nigra lectin (SNA); and immunohistochemistry for Gal-1, Gal-3, carbonic anhydrase IX, hypoxia-inducible factor, estrogen receptor (ER), progesterone receptor and human epidermal growth factor receptor type-2 for 86 IDC samples. Patients with markers positive for hypoxia were mostly ER-negative (p = 0.003) and presented with more nodal invasion than the non-hypoxic group (p = 0.0439). Concerning the glycobiological aspects, the hypoxic group expressed more of Gal-3 (p = 0.0021) and SNA ligands (p = 0.0498), however, there was no association between lectin-and galectin-staining and clinical and histopathological data. Our results suggest a change in the glycomic profile of patients within hypoxic regions of IDC. However, further studies are needed to evaluate the role of lectin-and galectin-ligands in tumor's hypoxic environment, as well as their potential to be used as therapeutic targets. (Folia Histochemica et Cytobiologica 2014, Vol. 52, No. 2, 96-103) Key words: breast cancer; IDC; hypoxia; glycomic profile; galectins; lectin ligands; IHC; histochemistry Ĩ ntroduction Breast cancer is the most common cancer among women, accounting for 22% of new cases every year, and the second most common cancer world wide [1]. Moreover, as with most solid tumors, breast cancers often have central regions of hypoxia which are usually peri-necrotic [2]. Cells that survive in this adverse environment are typically resistant to radiotherapy and chemotherapy and differ from cells in areas with adequate blood supply [3,4]. Hypoxia-inducible factor 1a (HIF-1a) is the major modulator of hypoxic condition and is constitutively produced under low-oxygen conditions, which typically occurs at distances greater than 180 μm from blood vessel [5]. HIF-1a affects tumor progression and angiogenesis by modulating the expression of genes involved in the adaptation to oxygen-and nutrient-deficiency, leading to increased cell survival, inhibition of apoptosis and migration [6,7]. Among these genes, carbonic anhydrase IX (CA IX) and glucose transporter 1 (GLUT1) play crucial roles in cellular adaptation, by altering the energy metabolism of neoplastic cells, which begin to show high rates of anaerobic glycolysis [2,[5][6][7]. The change in metabolic profile is followed by altered expression of enzymes involved in aerobic and anaerobic glycolysis, sugar
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