1,156 research outputs found
"There are millions of young Indians who feel frustrated with their lives.... I really want the Indian government to take these frustrations seriously." - Snigdha Poonam
No full textLSE South Asia Centre recently invited Snigdha Poonam, journalist at Hindustan Times and author of Dreamers: How Young Indians are Changing the World, for a panel discussion entitled 'Who are the Middle Class in South Asia?' as part of the South Asia Summit 2018. In conversation with Anirbaan Banerjee, she talks about aggressive Indian nationalism, the political and economic frustrations of the middle-class young Indian, women's aspirations and a growing social-political crisis in India
A Stacked Segmented Adaptive Power Amplifier in 22nm FD-SOI
No full textThis work was supported by Soitec. (Corresponding author: Aritra Banerjee.
Abstract 5891: DCIS to invasive progression in breast cancer is delayed by restoring CCN5
No full textAbstract
Malignant progression of breast cancer from pre-invasive to invasive lesions remains a mechanistically unknown event and a major challenge in medical research. By revealing the mechanism of action, our new and substantially different approach aims to demonstrate that CCN5/WISP2 might play a role in negative regulation of progression of pre-invasive lesion ductal carcinoma in-situ (DCIS) to invasive carcinoma (IC). DCIS to IC transition results primarily from the loss of the myoepithelial cell (MEC) layer surrounding the breast ducts & lobules and basement membrane (BM) degradation followed by invasion of cancer cells into the surrounding stromal tissue and vasculature. It has been recently discovered that CCN5, a matricellular protein, is highly expressed in DCIS patient specimens and facilitates regression of aggressive phenotypes. Our in-vitro studies with myoepithelial cell lines (MECs) indicate that CCN5 may prevent the DCIS to IC transition through the protection of the MEC layer. CCN5 performs it’s protective role by regulating sonic hedgehog (SHh) expression in MECs. It has been previously shown in separate studies that Neuropilin1 (Nrp1) positively regulates expression of SHh and Nrp1 is exclusively expressed in MEC layer in breast tissues. An extension of our studies indicate that CCN5 might regulate the integrity of the mammary ductal architecture by protecting the MEC layer through a novel Nrp1-SHh signaling axis. Collectively, our studies indicate that regulating CCN5 expression level in breast cancer tissues might help us controlling the rate of progression of the disease from DCIS to an invasive stage.
Citation Format: Sandipto Sarkar, Arnab Ghosh, Gargi Maity, Snigdha Banerjee, Sushanta Banerjee. DCIS to invasive progression in breast cancer is delayed by restoring CCN5 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5891. doi:10.1158/1538-7445.AM2017-5891</jats:p
Abstract 2118: The food additive agent potassium bromate prevents growth and aggressive phenotypes by targeting multiple molecular signatures in breast cancer cells
No full textAbstract
Potassium bromate (KBrO3) is by-product of ozone that has found multifunctional purpose in modern society. It is used as disinfectant in drinking water, a bleaching agent to improve flour, a component of cold-wave hair lotion and an ingredient in the production of fish paste and fermented beverages. Potassium bromide has also been used in America for bread-baking as a safe food additive since 1914. Despite the commercial value of this chemical, some studies suggest that KBrO3 could be a carcinogen. During the bread-baking process, Potassium bromate is normally converted into a stable and inert compound, potassium bromide (KBr). However, due to incomplete reduction, the residual KBrO3 remains in the bread, which eventually acts as a potential carcinogen to humans. Interestingly, our studies, in breast cancer cells, found contrasting results. We found that KBrO3 delays growth of ER-α positive luminal type breast cancer cells and triple-negative breast cancer cells (TNBC) via inducing apoptosis in a dose-dependent manner. KBrO3-induced apoptosis is mediated via targeting BCL-2/Bax and Caspase-3 signaling pathway. Moreover, aggressive phenotypes such as migration, invasion and sphere-forming ability of breast cancer cells are significantly impaired by KBrO3-treatment via targeting multiple molecular signatures in breast cancer cells. The growth inhibition effect of KBrO3 is also documented in a tumor xenograft model. Collectively, our findings provide a rationale for the basic and pre-clinical evaluation of the role of KBrO3 in breast cancer progression and therapy.
Citation Format: Priyanka Ghosh, Gargi Maity, Snigdha Banerjee, Sushanta Banerjee. The food additive agent potassium bromate prevents growth and aggressive phenotypes by targeting multiple molecular signatures in breast cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2118. doi:10.1158/1538-7445.AM2017-2118</jats:p
Abstract 790: Regulation of tumor angiogenesis by low dose Aspirin
No full textAbstract
Background and Objective: Tumor angiogenesis is a pathophysiological process in which new blood vessels are formed in the primary tumor site or distant organs for the nourishment of cancer cells and metastatic growth. Thereby, targeting tumor angiogenesis is an important area of research for cancer therapy. Abnormal structure of blood vessels (i.e. leakiness due to abnormal lining of pericytes on the microvessels) is one of the critical features of tumor angiogenesis that sensitizes vascular cells to cytokines and helps circulating tumor cells to metastasize to distant organs. Our long term goal is to repurpose the drugs that may prevent tumor angiogenesis or normalize the vessels by repairing leakiness via recruiting pericytes or both. Our recent studies found that Aspirin (ASA) has the potency to inhibit breast cancer growth and metastasis, as well as reprogram the mesenchymal to epithelial transition (MET). Given the importance of ASA, we tested whether ASA may be able to regulate tumor angiogenesis.
Methods: To do so, we determined the effect of low dose ASA (1mM, which is equivalent to 80mg human dose), ASA-treated (2.5mM) conditioned media (231-CMASA) or vehicle-treated conditioned media (231-CMVT) of MDA-MB-231 cells on different endothelial cell physiology. These include endothelial cells’ migration towards serum using 3D modified Boyden chamber assay, in vitro capillary-like structure formation on Matrigel, cell permeability using in vitro endothelial permeability assay and interactions of pericytes-endothelial cells. We also determined the effect of ASA on various angiogenic factors associated with tumor angiogenesis. Finally, we determined the effect of ASA on in vivo tumor angiogenesis using in vivo Angiogenesis Assay (Trevigen)
Results and Conclusions: We found that 231-CMASA significantly blocks in vitro migration, the formation of in vitro capillary-like structures parallel with leakiness via incomplete interaction of pericytes and endothelial cells as compared to 231-CMASA. The antiangiogenic effect of ASA was also documented in in vivo assays. Mechanistically, ASA treatment blocks several angiogenic factors including VEGF-A that are associated with these three events, implicating a low dose of Aspirin is potentially therapeutic for breast cancer via blocking and normalizing tumor angiogenesis.
Citation Format: Jinia Chakraborty, Gargi Maity, Snigdha Banerjee, Sushanta K. Banerjee. Regulation of tumor angiogenesis by low dose Aspirin [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 790. doi:10.1158/1538-7445.AM2017-790</jats:p
Author Exchange
No full textAnthropologist Mukulika Banerjee and political scientist Sushmita Pati have a conversation about their recently published books set in rural Bengal and Delhi’s urban villages, respectively. They situate their analyses of the intersections between democracy, capitalism, urbanization, and globalization in events, relations, and cultures of the everyday. Their exchange offers important insights for how political subjectivities and social ties are differently constituted or, to use Banerjee’s term, “cultivated” in these two settings. The two books offer a fine-grained view of how active citizenship in rural and urban India is refracted through distinct social and institutional structures. India is home to some of the world’s largest cities while more than 900 million people continue to live in the countryside. Its democratic future is therefore inextricably tied to the evolution of political behavior and political economy in both contexts, and, as Banerjee and Pati’s joint response indicates, to how urban and rural dynamics shape each other through (but not only through) migrants and their networks.
Contents:
Review of Mukulika Banerjee’s \u27Cultivating Democracy: Politics and Citizenship in Agrarian India\u27 by Sushmita Pati
Response from Mukulika Banerjee
Review of Sushmita Pati’s \u27Properties of Rent: Community, Capital and Politics in Globalising Delhi\u27 by Mukulika Banerjee
Response from Sushmita Pati
Joint Commentary from Banerjee and Pat
Abstract 5520: CCN5/WISP-2 is a negative regulator of epithelial to mesenchymal transition and stemness in breast cancer
No full textAbstract
Background and Objective: Breast cancer is the most common cancer in women and a leading cause of cancer mortality in western countries. CCN5 (also known as Wnt-1-induced signaling protein-2 or WISP-2) is a 29-31-kDa matricellular protein that plays as a negative regulator of breast carcinoma. Our previous studies had shown the importance of CCN5/ WISP-2 in the suppression of breast and pancreatic cancer progression through the regulation of the invasive phenotypes. Considering the previous report, our aim is to investigate whether human recombinant CCN5 inhibit pathobiological events like epithelial to mesenchymal transition (EMT), migration and stemness in triple negative breast cancer cells.
Methods: To investigate the negative impact of CCN5 on EMT and stemness of TNBC, we performed several techniques like western blot, clonoogenic assay, soft agar assay, sphere formation assay etc.
Results and Conclusions: The exposure of triple negative human breast cancer cells (TNBC), MDA-MB-231 and HCC-70, to recombinant CCN5 (hrCCN5), resulted in a dose-dependent inhibition of cell-proliferation through the induction of apoptotic cell death. The treatment of hrCCN5 regulates various pathobiological events in breast cancer cells, such as reprogramming the mesenchymal to epithelial transition (MET) followed by reduction of stemness features as confirmed by sphere formation assay and delaying in vitro migration. Finally, treatment with hrCCN5 in TNBC cells significantly inhibited anchorage-dependent and independent growth of TNBC. Collectively, CCN5’s control of cancer cell physiology indicates that hrCCN5 has the potential of being used as a major therapeutic agent against triple negative breast cancer.
Citation Format: Gargi Maity, Amlan Das, Sandipto Sarkar, Snigdha Banerjee, Sushanta K. Banerjee. CCN5/WISP-2 is a negative regulator of epithelial to mesenchymal transition and stemness in breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5520. doi:10.1158/1538-7445.AM2017-5520</jats:p
Abstract 84: CCN1/Cyr61 regulation of gemcitabine-resistant phenotype in pancreatic cancer: involvement of CTGF and dCK
No full textAbstract
With an estimated half a million new cases and similar mortality rates for 2016, pancreatic ductal adenocarcinoma (PDAC) remains a life-threatening and challenging disease to diagnose and treat. As per American Cancer Society (ACS), varying efficacy in different patients has led to an increase in the mortality rate of PDAC. Gemcitabine (GEM) remains the drug of choice either alone or in combination, but is unsuccessful in reducing or curing PDAC in most patients. The limited efficacies of these drugs are due to the acquisition of chemo-resistant characteristics of PDAC. Although several molecular and physiological factors have been shown to correlate with the GEM-resistance, defined molecular mechanism(s) of GEM-resistance remains a mystery. Previous studies have shown that CCN1, which is overexpressed in PDAC and known to associate with PDAC progression, is critical for drug resistance. Here, we found that while the pancreatic cancer cell lines (i.e., Panc-1 and AsPC-1) in which CCN1 is overexpressed are typically GEM-resistant, the knocking down of CCN1 makes them sensitive to GEM. Mechanistic studies revealed that CCN1 regulates two important genes that are directly involved in regulation GEM-sensitivity in PDAC. These include cancer cell-secreted connective tissue growth factor (CTGF), a regulator of desmoplasia, and Deoxycytidine kinase (dCK), an enzyme that enhances gemcitabine sensitivity and efficacy in cancer cells. The deletion of CCN1 in PDAC cells blocks CTGF expression and under co-cultured conditions prevent the growth of alpha-smooth muscle actin (α-SMA)-positive stellate cells, which are required for desmoplastic growth in pancreatic cancers. CCN1 ablation upregulates dCK expression in PDAC cell lines as compared to CCN1 expressed PDAC cells. These two events enhance the anti-proliferative effect of GEM and can be rescued by CTGF-treatment or blocking dCK. In conclusion, CCN1 promotes GEM-resistance in PDAC cell through the regulation of CTGF and dCK and the mechanistic insights provided by these studies may help in designing future therapeutic strategies to combat PDAC.
Citation Format: Vijayalaxmi G. Gupta, Gargi Maity, Inamul Haque, Sushanta K. Banerjee, Snigdha Banerjee. CCN1/Cyr61 regulation of gemcitabine-resistant phenotype in pancreatic cancer: involvement of CTGF and dCK [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 84. doi:10.1158/1538-7445.AM2017-84</jats:p
Abstract 4915: Alcohol-induced reprogramming of tumor plasticity is mediated via suppression of CCN5 signaling in breast cancer cells
No full textAbstract
Background and Objective: The epidemiological and experimental studies suggest that alcohol consumption is associated with increased risk for breast cancer development and metastasis. However, the mechanisms of alcohol-induced breast cancer progression and metastasis remain unknown. In this study, we examined the roles of CCN5, a tumor suppressor gene in alcohol induced breast cancer cell migration/invasion, epithelial to mesenchymal transition (EMT) and stemness.
Methods: Estrogen receptor-positive (ER+) human breast cancer cell line MCF-7 and immortalized normal human epithelial breast cell line MCF-12A were treated with ethanol at various concentrations in the presence and absence of human recombinant human CCN5 protein (hrCCN5) . Invasive/migratory ability of treated and untreated cells was measured by Boyden chamber assays. The mRNA and protein expression level of CCN5 was determined by real-time qRT-PCR and Western blot. EMT and stemness markers were evaluated by Western blot. Single-cell suspensions from pre-treated cells were re-suspended at a density of 500 cells/ml mammocult media in ultralow attachment dishes. Number as well as the size of the mammosphere in specified experimental set-up was monitored and recorded alternate day for 8-10 days.
Results: The studies demonstrated that alcohol promotes significantly the invasive/migratory ability and EMT phenotypes of breast cancer cells through the suppression of CCN5. Interestingly, hrCCN5 protein treatment suppresses the effect of alcohol and reprograms MET (mesenchymal to epithelial transition). In addition, alcohol-induced mammosphere formation efficiency is also suppressed by hrCCN5 protein-treatment.
Conclusions: Our findings suggest that the CCN5 signaling plays a preventive role in alcohol-induced reprogramming of tumor plasticity in breast cancer cells.
Citation Format: Inamul Haque, Arvind Subramanian, Vijayalaxmi Gupta, Sandipto Sarkar, Snigdha Banerjee, Sushanta K. Banerjee. Alcohol-induced reprogramming of tumor plasticity is mediated via suppression of CCN5 signaling in breast cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4915. doi:10.1158/1538-7445.AM2017-4915</jats:p
Banerjee_QSurvey_RawDataSet_PPC
No full textRaw dataset for questionnaire survey study (kinesiology taping_cancer care continuum)Author: Gourav Banerjee et alJournal: Progress in Palliative Care</div
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