Globalization and performance of microfinance institutions in the Philippines, Indonesia, and Cambodia for the periods 2004-2013

The researchers have examined how social and economic globalization affects MFI performance. As developed countries were able to cope with globalization, the researchers would want to know how globalization has an impact to microfinance institutions most especially in emerging countries such as the Philippines, Indonesia and Cambodia. The results of the study show that social and economic globalization somehow has a positive effect on an MFI\u27s return on assets. Operational self sufficiency is affected by economic globalization. On the other hand, social and economic globalization do not have significant effects on average loan and number of borrowers. The study also shows that there are other factors that contribute to the performance of MFIs including capital asset ratio, gross domestic product, efficiency, size, risk, age, inflation and female borrowers rate. The study therefore contributes to the growing knowledge of the effects of globalization in relation to microfinance institutions

NF-kB-mediated the expression of TBX15 in cancer cells

TBX15 is a T-box transcription factor essential for development, also proposed as a marker in prostate cancer; and, recently, its antiapoptotic function indicates a role in carcinogenesis. Regulation of TBX15 is uncovered. In this study, we investigated the regulation of TBX15 expression in human cancer cells, by analyzing the regulatory function of a 5'-distal conserved region of TBX15. Bisulfite sequencing showed high methylation of the CpG island contained in this region that was not correlated with TBX15 mRNA levels, in the cancer cell lines analyzed; however, after 5-aza-dC treatment of TPC-1 cells an increase of TBX15 expression was observed. We also found a significant response of TBX15 to TNF-α activation of the NF-κB pathway using five cancer cell lines, and similar results were obtained when NF-κB was activated with PMA/ionomycin. Next, by luciferase reporter assays, we identified the TBX15 regulatory region containing two functional NF-κB binding sites with response to NF-κBp65, mapping on the -3302 and -3059 positions of the TBX15 gene. Moreover, a direct interaction of NF-κBp65 with one of the two NF-κB binding sites was indicated by ChIP assays. In summary, we provide novel data showing that NF-κB signaling up-regulates TBX15 expression in cancer cells. Furthermore, the link between TBX15 and NF-κB found in this study may be important to understand cancer and development processes

NF-kB-mediated the expression of TBX15 in cancer cells

TBX15 is a T-box transcription factor essential for development, also proposed as a marker in prostate cancer; and, recently, its antiapoptotic function indicates a role in carcinogenesis. Regulation of TBX15 is uncovered. In this study, we investigated the regulation of TBX15 expression in human cancer cells, by analyzing the regulatory function of a 5'-distal conserved region of TBX15. Bisulfite sequencing showed high methylation of the CpG island contained in this region that was not correlated with TBX15 mRNA levels, in the cancer cell lines analyzed; however, after 5-aza-dC treatment of TPC-1 cells an increase of TBX15 expression was observed. We also found a significant response of TBX15 to TNF-α activation of the NF-κB pathway using five cancer cell lines, and similar results were obtained when NF-κB was activated with PMA/ionomycin. Next, by luciferase reporter assays, we identified the TBX15 regulatory region containing two functional NF-κB binding sites with response to NF-κBp65, mapping on the -3302 and -3059 positions of the TBX15 gene. Moreover, a direct interaction of NF-κBp65 with one of the two NF-κB binding sites was indicated by ChIP assays. In summary, we provide novel data showing that NF-κB signaling up-regulates TBX15 expression in cancer cells. Furthermore, the link between TBX15 and NF-κB found in this study may be important to understand cancer and development processes

Expression of <i>TBX15</i>mRNA and <i>CXCL1</i>mRNA in BHT cell lines after stimulation with TNF-α and PMA/I.

<p>(A) qRT-PCR of <i>TBX15</i>mRNA analysis in BHT and BHT IkBαSR cells after 3h of TNF-α or PMA/I treatment. (B) qRT-PCR of <i>CXCL1</i>mRNA analysis in BHT and BHT IkBαSR cells after 3h of TNF-α or PMA/I treatment. Data were normalized to <i>RPL27</i> and expressed as fold change referred to untreated cells whose <i>TBX15</i>mRNA or <i>CXCL1</i>mRNA relative expression was defined as 1. Data are mean ± SD of mRNA levels in triplicates. ** indicates p-value < 0.01.</p

Expression of <i>TBX15</i>mRNA in different cell lines after stimulation with TNF-α.

<p>(A) qRT-PCR of <i>TBX15</i>mRNA analysis in FRO, CGTH, TPC-1 and HeLa cells after 2h of TNF-α treatment. (B) qRT-PCR of <i>TBX15</i>mRNA (left) and <i>CXCL1</i>mRNA (right) analysis in p65^+/+ and p65^<i>-/-</i> MEF cells after TNF-α treatment. Data were normalized to <i>RPL27</i> and expressed as fold change referred to untreated cells whose <i>TBX15</i>mRNA or <i>CXCL1</i>mRNA relative expression was defined as 1. Data are mean±SD of mRNA levels of two independent experiments in triplicates. ** indicates p-value < 0.01.</p

Chromatin inmunoprecipitation (ChIP) assays.

<p>(A) The PCR amplified regions comprising the predicted NFκB binding sites (kBS1, kBS2 and kBS3) are indicated as rectangles, with location of these specific DNA segments indicated by numbers. (B) TPC and CGTH cells were treated with TNF-α and ChIP assays performed using IgG (mock) and NFκBp65 antibodies. Imnmunoprecipitated DNA was analyzed by qPCR with primers targeted to the predicted NFκB binding sites (kBS1, kBS2 and kBS3). The quantitative data reflect occupancy calculated as % input and represented as mean±SD of two independent experiments. *: P<0.05; **: P<0.01.</p

Identification of functional NF-κB responsive elements in the 5’-flanking region of the human <i>TBX15</i> gene.

<p>(A) Location and sequence of the predicted NF-κB binding sites (kBS1, kBS2 and kBS3) in the studied region of the <i>TBX15</i> promoter, with indication of altered sequence in mutated reporter constructs (underlined). Site directed mutagenesis was performed using P2 reporter construct to obtain the mutated reporter constructs. (B) Luciferase analysis of each mutated reporter constructs. <i>Left panel</i>, co-tansfected with the pCDNA3-p65 expression vector (p65) or the pCDNA3 empty vector (EV). <i>Right panel</i>, in nonstimulated or stimulated TNF-α cells. At least three independent experiments were performed with duplicates. Bars represent the mean±SD. * indicates p-value < 0.05 and ** p-value < 0.01.</p