Adaptive dewarping of severely warped camera-captured document images based on document map generation.

Automated dewarping of camera-captured handwritten documents is a challenging research problem in Computer Vision and Pattern Recognition. Most available systems assume the shape of the camera-captured image boundaries to be anywhere between trapezoidal and octahedral, with linear distortion in areas between the boundaries for dewarping. The majority of the state-of-the-art applications successfully dewarp the simple-to-medium range geometrical distortions with partial selection of control points by a user. The proposed work implements a fully automated technique for control point detection from simple-to-complex geometrical distortions in camera-captured document images. The input image is subject to preprocessing, corner point detection, document map generation, and rendering of the de-warped document image. The proposed algorithm has been tested on five different camera-captured document datasets (one internal and four external publicly available) consisting of 958 images. Both quantitative and qualitative evaluations have been performed to test the efficacy of the proposed system. On the quantitative front, an Intersection Over Union (IoU) score of 0.92, 0.88, and 0.80 for document map generation for low-, medium-, and high-complexity datasets, respectively. Additionally, accuracies of the recognized texts, obtained from a market leading OCR engine, are utilized for quantitative comparative analysis on document images before and after the proposed enhancement. Finally, the qualitative analysis visually establishes the system's reliability by demonstrating improved readability even for severely distorted image samples.

miR-590-3p inhibits proliferation and promotes apoptosis by targeting activating transcription factor 3 in human breast cancer cells.

We previously reported that ATF3 and Runx2 are involved in breast cancer progression and bone metastasis. The expression of these genes can be controlled by post-transcriptional regulators such as microRNAs (miRNAs). In this study, we identified and validated the functional role of miR-590-3p in human breast cancer cells (MDA-MB231). There was an inverse correlation between the expression of miR-590-3p and its putative target genes, ATF3 and Runx2 in these cells. Overexpression of miR-590-3p decreased the expression of ATF3 and Runx2 at the mRNA and protein levels in MDA-MB231 cells. Luciferase reporter assay identified a direct interaction of 3' UTRs of ATF3 and Runx2 with miR-590-3p in these cells. Overexpression of miR-590-3p also decreased proliferation and increased apoptosis of breast cancer cells. Based on our results, we suggest that miR-590-3p might have potential clinical applications towards controlling breast cancer progression and bone metastasis.

MicroRNA-590-5p Stabilizes Runx2 by Targeting Smad7 During Osteoblast Differentiation.

Mesenchymal stem cells (MSCs) are multipotent cells and their differentiation into the osteoblastic lineage is strictly controlled by several regulators, including microRNAs (miRNAs). Runx2 is a bone transcription factor required for osteoblast differentiation. Here, we used in silico analysis to identify a number of miRNAs that putatively target Runx2 and its co-factors to mediate both positive and negative regulation of osteoblast differentiation. Among these miRNAs, miR-590-5p was selected and its expression was found to be increased during osteoblast differentiation. When mouse MSCs (mMSCs) were transiently transfected with a miR-590-5p mimic, we detected an increase in both calcium deposition and the mRNA expression of osteoblast differentiation marker genes such as alkaline phosphatase (ALP) and type I collagen genes. Smad7 was found to be among the putative target genes of miR-590-5p and its mRNA and protein expression decreased after miR-590-5p mimic transfection in human osteoblast-like cells (MG63). Our analysis indicated that Runx2 was not a putative target of miR-590-5p. However, Runx2 protein, but not mRNA expression, increased after miR-590-5p mimic transfection in MG63 cells. Runx2 protein expression was increased with knockdown of Smad7 expression by Smad7 siRNA in these cells. We further identified that the 3'-untranslated region of Smad7 was directly targeted by miR-590-5p; this was done using the luciferase reporter gene system. It is known that Smad7 inhibits osteoblast differentiation via Smurf2-mediated Runx2 degradation. Hence, based on our results, we suggest that miR-590-5p promotes osteoblast differentiation by indirectly protecting and stabilizing the Runx2 protein by targeting Smad7 gene expression. J. Cell. Physiol. 232: 371-380, 2017. © 2016 Wiley Periodicals, Inc.

Transforming growth factor-ß1 regulation of ATF-3, c-Jun and JunB proteins for activation of matrix metalloproteinase-13 gene in human breast cancer cells.

Transforming growth factor-beta1 (TGF-ß1) plays a significant role in breast cancer mediated bone metastasis, and it stimulated expression of matrix metalloproteinase-13 (MMP-13; an invasive and metastasis gene) via activating transcription factor-3 (ATF-3) in human breast cancer cells (MDA-MB231). We further dissected the role of ATF-3 and its interacting proteins (activator protein-1; AP-1) for TGF-ß1-stimulation of MMP-13 expression in these cells. Chromatin immunoprecipitation (ChIP) experiment identified the TGF-ß1-stimulation of ATF-3 interaction at the AP-1 site of the MMP-13 promoter in a sustained and prolonged manner in MDA-MB231 cells. In silico protein-protein interaction, co-immunoprecipitation and western blot experiments identified the ATF-3 interaction and regulation of c-Jun and JunB proteins in these cells. The sequential ChIP assay confirmed the presence of c-Jun/ATF-3 complex at the AP-1 site of the MMP-13 promoter in MDA-MB231 cells upon TGF-ß1-treatment. Hence, our results suggested that TGF-ß1-treatment stimulated a sustained and prolonged expression of ATF-3, and its interaction and regulation of c-Jun protein and their assembly as a protein complex at the AP-1 site of the MMP-13 promoter could be responsible for MMP-13 gene activation in MDA-MB231 cells.

Runx2, a target gene for activating transcription factor-3 in human breast cancer cells.

Activating transcription factor (ATF-3) is a stress response gene and is induced by transforming growth factor beta 1 (TGF-ß1) in breast cancer cells. In this study, we dissected the functional role of ATF-3 gene in vitro by knocking down its expression stably in human bone metastatic breast cancer cells (MDA-MB231). Knockdown of ATF-3 expression in these cells decreased cell number, altered cell cycle phase transition, and decreased mRNA expression of cell cycle genes. Knockdown of ATF-3 expression in MDA-MB231 cells also decreased cell migration, and the expression levels of invasive and metastatic genes such as MMP-13 and Runx2 were found to be decreased in these cells. Most importantly, ATF-3 was associated with Runx2 promoter in MDA-MB231 cells and knockdown of ATF-3 expression decreased its association with Runx2 promoter. Hence, our results suggested that ATF-3 plays a role in proliferation and invasion of bone metastatic breast cancer cells in vitro and we identified for the first time that Runx2 is a target gene of ATF-3 in MDA-MB231 cell line.