Soil moisture change analysis under watershed management practice using in situ and remote sensing data in a paired watershed.

Soil moisture, vegetation cover, and land surface temperature are vital variables in water-energy balance, eco-hydrological processes, and water resources management, which can be influenced by watershed management activities. This research focused on the spatial and temporal variability of soil moisture, vegetation cover, land surface temperature, and Temperature-Vegetation Dryness Index (TVDI) under a biological watershed management practice in the Taleghan paired watershed, namely, treated (TW) and control watersheds (CW), in Alborz province, Iran. In this research, along with the remote sensing techniques, the soil moisture and vegetation cover data were measured and statistically analyzed in the three aspects of both TW and CW during a growth period from May to October 2017. The results indicated that soil moisture, vegetation cover, and land surface temperature values in the paired watershed were significantly different at the 0.01 level during the study period. The increased vegetation cover in the TW had an inverse effect on the land surface temperature and TVDI, while directly impacted the soil moisture content. The average TVDI in the CW was 0.83, while this index was found to be 0.69 in the TW. Unlike the vegetation cover and soil moisture, the results revealed that the southern aspects had the highest TVDI and land surface temperature compared to the northern and eastern aspects of both watersheds. However, the increased vegetation cover as a biological watershed management activity in the steep terrain and mountainous areas of TW led to an increased soil moisture and a decreased land surface temperature and soil dryness. As a result, decreasing soil dryness in the TW can exert vital controls on the water resources and increasing water availability. In the arid and semiarid countries such as Iran, a proper watershed management activity can effectively increase soil moisture and water availability in the watersheds. In particular, the vegetation cover protection and biological practices can be considered as practical solutions in the rehabilitation of exhausted watersheds in arid and semiarid environments.

MicroRNA-126 suppresses proliferation of undifferentiated (BRAF(V600E) and BRAF(WT)) thyroid carcinoma through targeting PIK3R2 gene and repressing PI3K-AKT proliferation-survival signalling pathway.

BACKGROUND: The objectives of this study are to investigate the expression of miR-126 and evaluate its effect on proliferation in undifferentiated thyroid carcinoma. METHODS: miR-126 expression of undifferentiated thyroid carcinoma cell lines 8505C (BRAF(V600E/V600E)), BHT-101 (BRAF(V600E/WT)) and MB-1 (BRAF(WT/WT)) were quantified with q-PCR. These cell lines were transiently transfected with exogenous miR-126 (mimic). Following transfection, proliferation effects were observed through MTS proliferation assay and colony formation abilities. Immunofluorescence imaging and Western blot assay were also done to check target proteins expression. RESULTS: Under-expression (p<0.05) of miR-126 was noted in BRAF(V600E) mutated undifferentiated thyroid carcinoma cells (8505C and BHT-101), but no change in expression was noted in non BRAF(V600E) mutated undifferentiated thyroid carcinoma cells (MB-1). In addition, a 30-50% drop in proliferation ability and a 35-45% reduction in colony formation capability were noticed in miR-126 mimic transfected group when compared to control group. Furthermore, immunofluorescence images showed reduced expression of p85ß and p-AKT protein in miR-126 mimic transfected cells when compared to un-transfected cells. Also, Western blot analysis revealed a 34-40% suppression of p85ß protein and a 21-53% drop in active AKT kinase (p-AKT) protein in miR-126 mimic transfected group when compared to control group. CONCLUSIONS: Expression of miR-126 was down-regulated in BRAF(V600E) mutated undifferentiated thyroid carcinoma. In addition, miR-126 was found to act as proliferation suppressor targeting PIK3R2 gene and reducing p85ß (a regulatory subunit of PI3K kinase) protein translation and lower AKT kinase activity. Therefore, miR-126 could be a potential therapeutic tool in the treatment of undifferentiated thyroid carcinoma.

A combination of traditional learning and e-learning can be more effective on radiological interpretation skills in medical students: a pre- and post-intervention study.

BACKGROUND: The ability to interpret an X-Ray is a vital skill for graduating medical students which guides clinicians towards accurate diagnosis and treatment of the patient. However, research has suggested that radiological interpretation skills are less than satisfactory in not only medical students, but also in residents and consultants. METHODS: This study investigated the effectiveness of e-learning for the development of X-ray interpretation skills in pre-clinical medical students. Competencies in clinical X-Ray interpretation were assessed by comparison of pre- and post-intervention scores and one year follow up assessment, where the e-learning course was the 'intervention'. RESULTS: Our results demonstrate improved knowledge and skills in X-ray interpretation in students. Assessment of the post training students showed significantly higher scores than the scores of control group of students undertaking the same assessment at the same time. CONCLUSIONS: The development of the Internet and advances in multimedia technologies has paved the way for computer-assisted education. As more rural clinical schools are established the electronic delivery of radiology teaching through websites will become a necessity. The use of e-learning to deliver radiology tuition to medical students represents an exciting alternative and is an effective method of developing competency in radiological interpretation for medical students.

Multiple proliferation-survival signalling pathways are simultaneously active in BRAF V600E mutated thyroid carcinomas.

BACKGROUND AND OBJECTIVES: BRAF is an oncogene which involves in pathogenesis of many thyroid carcinomas.The aim of our study was to investigate whether the downstream signalling pathway of BRAF and AKT kinase signalling pathways were active in BRAF V600E mutated thyroid carcinoma cells. METHODS: Five thyroid (papillary and undifferentiated) carcinoma cell lines and one non-cancer thyroid cell line were screened for their BRAF V600E mutation status by immunofluorescent staining and Western blot. BRAF V600E mutated thyroid carcinoma cell lines were used to test the activation status of both ERK and AKT kinase proteins through immunofluorescent studies and Western blots. RESULTS: Expressions of BRAF V600E mutated protein were confirmed in four thyroid (papillary and undifferentiated) carcinoma cell lines. In these cell lines, both active ERK and active AKT kinase proteins were found in BRAF V600E mutated thyroid carcinoma cells by immunofluorescent staining and Western blots experiments. CONCLUSIONS: In BRAF V600E mutated thyroid carcinomas, active ERK and active AKT kinase proteins were noted. They are able to stimulate multiple downstream signalling pathways which ultimately result in increased proliferation and survival activities for cancer cells. Therefore, consideration needs to put on multiple targets when deciding molecular target therapies for patients with BRAF V600E mutated thyroid carcinoma.

The roles of JK-1 (FAM134B) expressions in colorectal cancer.

The aims of the present study are to investigate the clinicopathological correlations of JK-1(FAM134B) expression and its relationship to carcinogenesis in a colorectal adenoma-adenocarcinoma model. JK-1(FAM134B) protein expression was studied in a colon cancer cell line by Western blot and immunocytochemistry. JK-1(FAM134B) expression profiles at mRNA and protein levels were investigated in cancer tissues from 236 patients with colorectal adenocarcinoma and 32 patients with colorectal adenoma using real-time polymerase chain reaction and immunohistochemistry. The findings were then correlated with the clinicopathological features of these tumours. JK-1(FAM134B) protein was demonstrated in the colon cancer cells by Western blot. The protein was located in the nuclei of the tumour cells at both cellular and tissue levels. In colorectal adenocarcinomas, lower levels of JK-1(FAM134B) protein expression were associated with younger age (p=0.032), larger tumour size (p=0.004), advanced cancer stages (p=0.016) and higher rates of cancer recurrence (p=0.04). Also, lower levels of JK-1(FAM134B) mRNA expression were associated with advanced cancer stages (p=0.02) and presence of lymphovascular invasion (p=0.014). Higher JK-1(FAM134B) mRNA and protein expression levels were identified in adenomas and non-neoplastic mucosae, compared to carcinomas (p=0.005). To conclude, JK-1(FAM134B) mRNA expression and JK1 (FAM134B) protein levels varied with the different stages of progression of colorectal tumours. The expression levels of the gene were associated with clinicopathological features in patients with colorectal adenocarcinoma suggesting that JK-1(FAM134B) gene has roles in controlling some steps in the development of the invasive phenotypes from colorectal adenoma to early staged as well as advanced staged colorectal adenocarcinomas.

Regulation of microRNA-1288 in colorectal cancer: altered expression and its clinicopathological significance.

We aim to examine the miR-1288 expression in cancer cell lines and a large cohort of patients with colorectal cancer. Two colon cancer cell lines (SW480 and SW48) and one normal colonic epithelial cell line (FHC) were recruited. The miRNA expressions of miR-1288 were tested on these cell lines by using quantitative real-time polymerase chain reaction (qRT-PCR). An exogenous miR-1288 (mimic) was used to detect cell proliferation and cell cycle changes in SW480 using MTT calorimetric assay and flow cytometry, respectively. In addition, tissues from 122 patients with surgical resection of colorectum (82 adenocarcinomas, 20 adenomas, and 20 non-neoplastic tissues) were tested for miR-1288 expression by qRT-PCR. The colon cancer cell lines showed reduced expression of miR-1288 compared to normal colonic epithelial cell line. Over expression of miR-1288 in SW480 cell line showed increased cell proliferation and increased G2-M phase cells. In tissues, reduced miR-1288 expression was noted in majority of colorectal adenocarcinoma compared to colorectal adenoma and non-neoplastic tissues. Reduced or absent expression of miR-1288 was noted in 76% (n = 62/82) of the cancers. The expression levels of miR-1288 were higher in distal colorectal adenocarcinomas (P = 0.013) and in cancers of lower T staging (P = 0.033). To conclude, alternation of miR-1288 expression is important in the progression of colorectal cancer. The differential regulation of miR-1288 was found to be related to cancer location and pathological staging in colorectal cancers.

Role of microRNA-34 family in cancer with particular reference to cancer angiogenesis.

MicroRNA-34 is involved in pathogenesis in cancer by targeting different tumor-related genes. It could be a biomarker for predicting the prognosis of patients with cancer. In addition, miR-34 is involved in the tumor angiogenesis. Understanding the mechanism of the miR-34 in cancer and tumor angiogenesis will open horizons for development of anti-cancer and anti-angiogenesis drugs.

JK1 (FAM134B) gene and colorectal cancer: a pilot study on the gene copy number alterations and correlations with clinicopathological parameters.

AIMS: The aims of the study are to characterize changes in JK-1 (FAM134B) at the DNA level in colorectal adenocarcinoma and adenoma and exploring the possible correlations with clinical and pathological features. METHOD: JK-1 gene DNA copy number changes were studied in 211 colorectal carcinomas, 32 colorectal adenoma and 20 colorectal non-cancer colorectal tissue samples by real-time quantitative polymerase chain reaction. The results were correlated with clinical and pathological parameters. RESULTS: Colorectal adenomas were more likely to be amplified than deleted with regard to JK-1 (FAM134B) DNA copy number change. The copy number level of JK-1 (FAM134B) DNA in colorectal adenocarcinomas was significantly lower in comparison to colorectal adenomas. Changes in JK-1 (FAM134B) DNA copy number were associated with histological subtypes, and cancer stage. Lower copy numbers were associated with higher tumor stage, lymph node stage and overall pathological stage of cancer. Conversely, higher DNA copy numbers were detected more often in the mucinous adenocarcinoma. CONCLUSIONS: This is the first study showing significant correlations of the JK-1 (FAM134B) gene copy number alterations with clinical and pathological features in a large cohort of pre-invasive and invasive colorectal malignancies. The changes in DNA copy number associated with progression of colorectal malignancies reflect that JK-1 (FAM134B) gene could play a role in controlling some steps in development of the invasive phenotypes.

JK1 (FAM134B) represses cell migration in colon cancer: a functional study of a novel gene.

BACKGROUND: JK1 is a novel cancer-related gene with unknown functional role in carcinogenesis. The aim of this study is to investigate the role of JK1 gene in carcinogenesis in an in vitro cell proliferation and migration analysis model. METHODS: Small hairpin RNAs (shRNA) were designed to knock-down JK1 expression in colon cancer cell line (SW480) using transduction ready lentiviral particles. Cell proliferation and cell migration assays were performed on multiple extracellular matrices to investigate the cellular effects of JK1 in colon cancer cells. A non-cancer colonic epithelial cell line (FHC) was used to compare the expression of JK1 in cancer cell line. RESULTS: JK1 knock-down did not affect cellular proliferation or survival in colon cancer. However, the manipulation increased cancer cell migration rates on collagen and fibronectin substrates. CONCLUSIONS: JK1 was shown for the first time to have a functional role in the pathogenesis of colon cancer. The results imply that JK1 represses the capacity of cancer cells to migrate within their tissue. They also concurred with the previous findings of JK1 activity correlations with clinical and pathological features in colon cancer. The capacity may have utility as a means to prevent cancer cells forming metastases.

The expression profiles of the galectin gene family in primary and metastatic papillary thyroid carcinoma with particular emphasis on galectin-1 and galectin-3 expression.

INTRODUCTION: Galectin family members have been demonstrated to be abnormally expressed in cancer at the protein and mRNA level. This study investigated the levels of galectin proteins and mRNA expression in a large cohort of patients with papillary thyroid carcinoma and matched lymph node metastases with particular emphasis on galectin-1 and galectin-3. METHODS: mRNA expression of galectin family members (1, 2, 3, 4, 7, 8, 9, 10 and 12) were analysed by real-time polymerase chain reaction in 65 papillary thyroid carcinomas, 30 matched lymph nodes with metastatic papillary thyroid carcinoma and 5 non-cancer thyroid tissues. Galectin-1 and 3 protein expression was determined by immunohistochemistry in these samples. RESULTS: Significant expression differences in all tested galectin family members (1, 2, 3, 4, 7, 8, 9, 10 and 12) were noted for mRNA in papillary thyroid carcinomas, with and without lymph node metastasis. Galectin-1 protein was more strongly expressed than galectin-3 protein in papillary thyroid carcinoma. Galectin-1 protein was found to be overexpressed in 32% of primary papillary thyroid carcinomas. A majority of lymph nodes with metastatic papillary thyroid carcinoma (53%) had significantly increased expression of galectin-1 protein, as did 47% of primaries with metastases. Galectin-1 mRNA levels were decreased in the vast majority (94%) of primary thyroid carcinomas that did not have metastases present. Galectin-3 protein levels were noted to be overexpressed in 15% of primary papillary thyroid carcinomas. In primary papillary thyroid carcinoma with lymph node metastases, 32% had over expression of galectin-3 protein. Overexpression of galectin-3 mRNA was noted in 58% of papillary thyroid carcinomas and 64% of lymph nodes bearing metastatic papillary thyroid carcinoma. Also, primary papillary thyroid carcinoma with lymph node metastases had significantly higher expression of galectin-3 mRNA compared to those without lymph node metastases. CONCLUSION: Galectin family members show altered expression at the mRNA level in papillary thyroid cancers. Overexpression of galectin-1 and 3 proteins were noted in papillary thyroid carcinoma with lymph node metastases. The results presented here demonstrated that galectin-1 and galectin-3 expression have important roles in clinical progression of papillary thyroid carcinoma.

Expression profile of endothelin 1 and its receptor endothelin receptor A in papillary thyroid carcinoma and their correlations with clinicopathologic characteristics.

The endothelin axis is a group of signaling molecules and their receptors that have been implicated in vascularization of cancers, with their expression being observed to change in different cancer types. In this research, we examined the expression of endothelin 1 and endothelin receptor A at the protein and messenger RNA (mRNA) levels in 123 papillary thyroid carcinomas and 40 matched lymph nodes with metastatic papillary thyroid carcinomas. We found altered endothelin axis mRNA expression in several clinicopathologic parameters with increased endothelin 1 expression in thyroid papillary carcinoma showing stromal calcification, cancers in men, and primary cancers with lymph node metastases. Increased endothelin receptor A mRNA expression was noted in the larger cancers. There is a significant correlation between expression of endothelin receptor A and endothelin 1 in papillary thyroid carcinoma. Both endothelin receptor A and endothelin 1 mRNA expressions were significantly higher in metastatic carcinoma in the lymph node than in primary thyroid cancer. The metastatic carcinoma in the lymph node had increased expression compared with matched primary thyroid carcinoma. Expressions of endothelin 1 and endothelin receptor A were also documented as being high at the protein level. Our results indicate that in thyroid cancer, endothelin 1 and endothelin receptor A are associated with growth in advanced stages and lymph node metastases, likely through known angiogenic linkages. Targeting the endothelin axis may be useful in planning angiogenesis therapy for thyroid cancer.

Orofacial viral infections--an update for clinicians.

UNLABELLED: Orofacial viral infections may be less common but appear in different clinical forms. Often these infections get initially treated by antibiotics which obviously will have limited or no effect. The authors review the current concepts of orofacial viral infections, causative agents, their classification and clinical manifestations and a basis for treatment. CLINICAL RELEVANCE: Most viral infections do not require any specific treatment except in patients who are immunosuppressed or immunodeficient. Appropriate diagnosis and timely management of orofacial viral lesions are important irrespective of whether it is localized or a manifestation of a systemic infection.

Myeloma-induced alloreactive T cells arising in myeloma-infiltrated bones include double-positive CD8+CD4+ T cells: evidence from myeloma-bearing mouse model.

The graft-versus-myeloma (GVM) effect represents a powerful form of immune attack exerted by alloreactive T cells against multiple myeloma cells, which leads to clinical responses in multiple myeloma transplant recipients. Whether myeloma cells are themselves able to induce alloreactive T cells capable of the GVM effect is not defined. Using adoptive transfer of T naive cells into myeloma-bearing mice (established by transplantation of human RPMI8226-TGL myeloma cells into CD122(+) cell-depleted NOD/SCID hosts), we found that myeloma cells induced alloreactive T cells that suppressed myeloma growth and prolonged survival of T cell recipients. Myeloma-induced alloreactive T cells arising in the myeloma-infiltrated bones exerted cytotoxic activity against resident myeloma cells, but limited activity against control myeloma cells obtained from myeloma-bearing mice that did not receive T naive cells. These myeloma-induced alloreactive T cells were derived through multiple CD8(+) T cell divisions and enriched in double-positive (DP) T cells coexpressing the CD8αα and CD4 coreceptors. MHC class I expression on myeloma cells and contact with T cells were required for CD8(+) T cell divisions and DP-T cell development. DP-T cells present in myeloma-infiltrated bones contained a higher proportion of cells expressing cytotoxic mediators IFN-γ and/or perforin compared with single-positive CD8(+) T cells, acquired the capacity to degranulate as measured by CD107 expression, and contributed to an elevated perforin level seen in the myeloma-infiltrated bones. These observations suggest that myeloma-induced alloreactive T cells arising in myeloma-infiltrated bones are enriched with DP-T cells equipped with cytotoxic effector functions that are likely to be involved in the GVM effect.

Towards a flood vulnerability assessment of watershed using integration of decision-making trial and evaluation laboratory, analytical network process, and fuzzy theories.

Among natural disasters, flood is increasingly recognized as a serious worldwide concern that causes the most damages in parts of agriculture, fishery, housing, and infrastructure and strongly affects economic and social activities. Universally, there is a requirement to increase our conception of flood vulnerability and to outstretch methods and tools to assess it. Spatial analysis of flood vulnerability is part of non-structural measures to prevent and reduce flood destructive effects. Hence, the current study proposes a methodology for assessing the flood vulnerability in the area of watershed in a severely flooded area of Iran (i.e., Kashkan Watershed). First interdependency analysis among criteria (including population density (PD), livestock density (LD), percentage of farmers and ranchers (PFR), distance to industrial and mining areas (DTIM), distance to tourist and cultural heritage areas (DTTCH), land use, distance to residential areas (DTRe), distance to road (DTR), and distance to stream (DTS)) was conducted using the decision-making trial and evaluation laboratory (DEMATEL) method. Hence, the cause and effect factors and their interaction levels in the whole network were investigated. Then, using the interdependency relationships among criteria, a network structure from flood vulnerability factors to determine their importance of factors was constructed, and the analytical network process (ANP) was applied. Finally, with the aim to overcome ambiguity, reduce uncertainty, and keep the data variability, an appropriate fuzzy membership function was applied to each layer by analyzing the relationship of each layer with flood vulnerability. Importance analysis indicated that land use (0.197), DTS (0.181), PD (0.180), DTRe (0.140), and DTR (0.138) were the most important variables. The flood vulnerability map produced by the integrated method of DEMATEL-ANP-fuzzy showed that about 19.2% of the region has a high to very high flood vulnerability.

Inhibition of BRAF kinase suppresses cellular proliferation, but not enough for complete growth arrest in BRAF V600E mutated papillary and undifferentiated thyroid carcinomas.

The aim of our study was to inhibit BRAF kinase expression and investigate its effect on cellular functions in thyroid carcinomas. 8505C (BRAF V600E/V600E) undifferentiated thyroid carcinoma cell line and B-CPAP (BRAF V600E/V600E) papillary thyroid carcinoma cell line were used to develop doxycycline-inducible anti-BRAF shRNA stable cell lines. The inhibitions of BRAF expression in these cells were confirmed with qPCR and Western blot. Impacts of BRAF protein inhibition on cellular functions and signalling pathways were observed through Western blot, proliferation and colony formation assays. BRAF kinase expression was inhibited 83 % in undifferentiated thyroid carcinoma and 82 % in papillary thyroid carcinoma (p < 0.05). As a result of BRAF kinase inhibition, reduction in MEK kinase activity was seen (p < 0.05) in both thyroid cancer cell lines (72 and 75 %, respectively). Initially, big drop in proliferation (p < 0.05) was observed (52 and 54 %, respectively), but later an increasing proliferation trend was noticed in BRAF kinase-inhibited cell lines. In addition, reduction in colony formation (p < 0.05) was seen in BRAF kinase-inhibited carcinoma cells (13 and 15 %, respectively). On the other hand, increase in AKT kinase activity (63 and 70 %, respectively; p < 0.05) was discovered in both BRAF kinase-inhibited carcinoma cells. Increased activation of alternative proliferation pathways (as determined by the increase of AKT kinase activity) counteracts the effect of BRAF kinase inhibition in thyroid carcinomas. Thus, alternative proliferation pathways should be inhibited for therapeutic suppression of BRAF-induced proliferation in thyroid carcinomas.

Interactive role of miR-126 on VEGF-A and progression of papillary and undifferentiated thyroid carcinoma.

MicroRNA-126 (miR-126) expression has been shown to be associated with angiogenesis. The aim of the current study is to evaluate the functional roles of miR-126 in dysregulation of VEGF expression and cancer progression in thyroid carcinomas. The expression of VEGF-A and miR-126 were measured in 101 thyroid carcinomas tissues (including 51 conventional papillary thyroid carcinoma, 37 follicular variant of papillary thyroid carcinoma, and 13 undifferentiated thyroid carcinomas), 13 matched lymph nodes with metastatic thyroid carcinoma, 21 benign thyroid tissues, and 5 thyroid carcinoma cell lines (both papillary and undifferentiated carcinomas). Then, exogenous miR-126 was transfected, and the expressions of VEGF-A were determined (Western blot technique). Proliferation assay, cell cycle analysis, and apoptosis assays were used to evaluate the role of miR-126 in these events. Significant underexpression of miR-126 levels in thyroid cancer tissues and cell lines was detected using real-time polymerase chain reaction. Introducing exogenous miR-126 into the cancer cell lines resulted in a significant reduction of VEGF-A protein expression. Marked inhibition in proliferation, cell cycle arrest in G0-G1, and promotion of total apoptosis were also noted. The modulatory role of miR-126 on expression of VEGF-A and its tumor suppressive roles were demonstrated for the first time in thyroid cancer. The current experiments provided specific information on the functional consequences of VEGF manipulation via microRNA on cancer.

The expression profiles of the galectin gene family in colorectal adenocarcinomas.

We aim to investigate the expression profiles of galectin family genes (galectins-1, 2, 3, 4, 7, 8, 9, 10, and 11) in colorectal carcinomas. Messenger RNA (mRNA) expression of galectin family members (1, 2, 3, 4, 7, 8, 9, 10, and 12) was analyzed by real-time polymerase chain reaction in colorectal tissues from 201 patients (54 noncancer colorectal tissues, 49 adenomas, and 98 adenocarcinomas). Galectin-1 and galectin-3 protein expressions were determined by immunohistochemistry. In general, high galectin mRNA expression was noted in colorectal carcinomas in early stages of their pathogenesis. Significant differences in galectins-2, 3, 7, 8, and 10 mRNA expression were associated with pathologic stages (P<.05). Increased prevalence of galectins-2, 7, 8, and 10 mRNA overexpression was noted in nonmetastatic colorectal carcinomas (P<.05). Galectin-1 and galectin-3 proteins were present in the nucleus and cytoplasm of the colorectal tissues and expressed significantly higher in colorectal carcinomas when compared to colorectal adenomas (61% and 95%, respectively). Patients with colorectal carcinoma with high levels of galectin-3 mRNA and protein expression showed better prognosis (P=.052). To conclude, many novel correlations between the deregulation of galectin family genes and various clinicopathological features in colorectal adenocarcinoma were noted. Overexpression of galectins at the mRNA level and proteins were predominant in earlier stages of colorectal carcinomas. These altered expression patterns of galectin genes suggest the multifunctional role of galectin genes in the regulation of colorectal cancer development, progression, and metastasis.

Modulatory role of miR-205 in angiogenesis and progression of thyroid cancer.

miR-205 plays a crucial role in angiogenesis and has been found in association with several types of cancers. The aims of this study were to investigate the clinical and functional roles of miR-205 on as the major initiator and modulator of angiogenesis in thyroid cancer. 101 thyroid carcinomas, including 51 conventional and 37 follicular variants of papillary thyroid carcinomas, and 13 undifferentiated thyroid carcinomas in addition to 13 lymph nodes with metastatic thyroid carcinoma were recruited to be compared with 14 nodular goitre and seven normal thyroid tissues. Five thyroid carcinoma cell lines, of papillary and undifferentiated origin with and without history of metastasis, were also used. Expression of vascular endothelial growth factor A (VEGFA) and miR-205 were measured and exogenous miR-205 were transfected to observe the changes of VEGFA (by immunofluorescence and western blot techniques). Proliferation assay, cell cycle analysis and apoptosis assays were also used to evaluate the role of miR-205 in these events. Significant under-expression of miR-205 and over-expression of VEGFA mRNA and protein were noticed in thyroid cancer tissues and cell lines compared to normal thyroid control. Transfection of miR-205 into the cancer cell lines caused significant reduction of VEGFA protein and significant inhibition in cell proliferation, arrest in G0-G1 of the cell cycle and promotion of total apoptosis (P<0.05). The angiogenic and tumour-suppressive roles of miRNA-205 were demonstrated for the first time in thyroid cancer. The current experiments provided specific information on the functional consequences of VEGF manipulation via miRNA on cancer.

MicroRNA-34 family, mechanisms of action in cancer: a review.

Altered expression of the microRNA-34 family has been determined to be involved in the pathogenesis of many cancers. In this review, the current knowledge of the cancer-related mechanisms in relation to the modulatory effects of microRNA-34 family were analysed. Expression analysis of the microRNA-34 family has suggested that its members play significant roles in many aspects of cancer biology including proliferation, invasion/metastasis, apoptosis/cell survival, cell cycle/cell growth, migration, senescence/aging, angiogenesis, epigenetic silencing and methylation by regulation of the expression of their target genes. Thus, microRNA-34 family members could act as prognostic markers and therapeutic targets in human cancers.

The important roles of miR-205 in normal physiology, cancers and as a potential therapeutic target.

Evidences have demonstrated key mediatory roles of microRNA-205 (miR-205) in normal physiology and its aberrant expression in many cancers. Indeed, miR-205 has been identified as both a tumour suppressive and oncogenic miRNA playing crucial roles in tumourigenesis through regulating different cellular pathways such as cell survival, apoptosis, angiogenesis and metastasis. As a tumour suppressor, miR-205 acts as an inhibitor of cell proliferation, migration and invasion. On the other hand, as an oncogene, miR-205 promotes tumour initiation and development. All these functions act through different target genes in various types of cancers. Also, miR-205 displays potential as a therapeutic target for different cancers. To conclude, miR-205 has important clinical and pathological correlations in different cancers and may act as a diagnostic and prognostic marker as well as new molecular target for cancer therapy.