Browsing by Author "Akanksha Pandey"
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PublicationArticle Contrasting nature of aerosols over South Asian cities and its surrounding environment(Elsevier Ltd, 2024) Akanksha Pandey; Kumari Aditi; Harshita Baranwal; Asfa Siddiqui; Tirthankar BanerjeeCross-country assessment of aerosol loading was made over several South Asian megacities using multiple high-resolution remote-sensing database to assess how aerosols vary within the city and its suburbs. Parameters sensitive to aerosol optical and microphysical properties were processed over city-core and its surrounding, separated by a buffer. Cities across the Indo-Gangetic Plain (IGP; AOD:0.52–0.72) along with Mumbai (0.47) and Bangalore (0.46) denote comparatively high aerosol loading against non-IGP cities. City-core specific AOD was invariably high compared to surrounding, however with varying gradient having robust geographical signature. Exceptions to this general trend were in Kathmandu (ΔAOD: 0.07) and Dhaka (ΔAOD: 0.01) while strong positive AOD gradient was noted in Bangalore (+0.11), Colombo (+0.08) and in Mumbai (+0.07). While all mainland cities exhibited robust intraannual variability, distinction between city-core and its surrounding AOD exhibited varying seasonality. City-specific geometric coefficient of variation indicated insignificant association with mean AOD as opposed to European and American cities. Both pixel-based and city-specific analysis revealed a strong increasing trend in AOD with highest magnitude in Varanasi and Bangalore. Aerosol sub-types based on aerosols’ sensitivity to UV-absorption and particle size denotes higher relative abundance of carbonaceous smoke aerosols within city-core, without having significant distinction for mineral dusts and urban aerosols. © 2024 Elsevier LtdPublicationArticle Fisetin induces apoptosis in colorectal cancer cells by suppressing autophagy and down-regulating nuclear factor erythroid 2-related factor 2 (Nrf2)(John Wiley and Sons Inc, 2023) Akanksha Pandey; Surendra Kumar TrigunModulation of autophagy is evolving as a relevant strategy in cancer pathogenesis and therapeutic intervention and hence, needs to be examined as a target for the promising anticancer agents. Fisetin, a dietary flavanol, is emerging as a potent anticancer agent, however, its tumour-specific pharmacological targets remain largely unexplored. This article describes correlative profiles of autophagy and apoptotic markers versus nuclear factor erythroid 2-related factor 2 (Nrf2) and reactive oxygen species (ROS) in the colorectal cancer (CRC) cell line SW-480. As compared to the untreated cells, significantly less number of fluorescent detected autophagic vacuoles (AVOs) in the fisetin-treated cells coincided with a similar decline of the autophagy flux markers, Beclin 1 and microtubule-associated protein-1 light chain-3 and accumulation of p62 in those cells. The significantly increased number of annexin-V/propidium iodide (+/+) positive and acridine orange/ethidium bromide-stained apoptotic cells coincided with the enhanced signals for the cleaved caspase 3 and nuclear PARP-1 in those fisetin-treated cells. This was consistent with the collapse of mitochondrial membrane potential and release of cytochrome c. The fisetin-treated cells showed increased ROS level and a significant decline in nuclear Nrf2 immunosignal versus recovery in nuclear Nrf2 due to the treatment with curcumin and resveratrol (Nrf2 activators) and thus, suggesting a role of Nrf2 suppression in fisetin-mediated apoptosis in SW-480 cells. The effect of chloroquine, an autophagy inhibitor, resulted into declined number of AVOs and enhanced apoptosis, similar to that of the fisetin effect. Also, regaining of AVOs number and reduced apoptosis of CRC cells due to the treatment with rapamycin, an autophagy inducer, could be observed. These loss and gain of functions experiments thus suggested a correlation between fisetin-mediated autophagy suppression and apoptotic induction in a colorectal cell line. © 2023 Wiley Periodicals LLC.PublicationArticle Forest fire emission estimates over South Asia using Suomi-NPP VIIRS-based thermal anomalies and emission inventory(Elsevier Ltd, 2025) Kumari Aditi; Akanksha Pandey; Tirthankar BanerjeeEmission estimates of carbon-containing greenhouse gases (CO2, CH4) and aerosols (PM2.5) were made from forest fire across South Asia using Visible Infrared Imaging Radiometer Suite (VIIRS) based thermal anomalies and fire products. VIIRS 375 m I-band active fire product was selectively retrieved for the years 2012–2021 over forest cover across South Asia. Annual incidence of fire events across South Asia was 0.17 (±0.05) million (M) with robust spatio-temporal variation. Fire occurrences were mainly concentrated over the forest across Hindu Kush Himalayan region (HKH; 56%), Deccan Plateau (DP) and Central Highlands (CH; 34%). Monthly mean fire incidences emphasize February to May as a typical forest fire season, accounting 90% of annual fire counts. The highest fire pixel density (>1.5 km −2 yr−1) was noted over the tropical dry/moist deciduous and tropical semi-evergreen forests. Strong diurnal nature of fire radiative power (FRP) was evident with >85% of FRP linked to daytime retrieval. VIIRS based Fire Emission Inventory (VFEI, Version 0) was followed to constitute regional emissions of PM2.5 and green house gases from forest fire. Forest fire accounted a yearly emission of 91.58 (±14.76) and 0.25 (±0.04) Tg yr−1 CO2 and CH4 respectively, with 25.14 (±3.94) Tg of cumulative carbon release per year, i.e., roughly 1.3% of global fire-related carbon emission. Fire associated PM2.5 emission rate was 0.60 (±0.10) Tg yr−1, 95% of which emitted during peak fire season as was the case for carbon-containing gases. Forest fire across HKH (75%) and DP + CH (20%) predominately contribute to the regional carbon emission, while also accounting 68% (HKH) and 27% (DP + CH) of fire associated PM2.5 emission budget. With >70% of forest fires within South Asia being typically anthropogenic, forest fire appears to be a major sector of greenhouse gas and aerosols emissions, and necessitate planning and strict legalities to reduce emission load. © 2024 Elsevier LtdPublicationBook Chapter Hyperglycolysis-Inflammation Connect as a Mechanistic Hot Spot in Oxidatively Compromised Cancer(Springer Nature, 2022) Brajesh Kumar Maurya; Akanksha Pandey; Surendra Kumar TrigunHyperglycolysis, as a major bioenergetics shift in the growing tumor cells, ensures adequate amount of ATP synthesis by avoiding mitochondrial oxidative mechanism and thereby protects tumor cells from reactive oxygen species (ROS)-induced cellular damage. Such an oxidatively compromised state of the tumor cells is considered crucial for making them immortal. The generation of pro-inflammatory factors around the tumor cells is advocated as another important event, and that, together with the hyperglycolysis, it constitutes a pro-tumorigenic tumor microenvironment (TME) and facilitates in vivo tumorigenesis. Herein, the enhanced lactate secretion, due to upregulated aerobic glycolysis, by the tumor stem cells (TSCs), acts as a key integrator of hyperglycolysis-inflammation connect. Consequently, dynamic interaction takes place between the TSC, the tumor-associated macrophages (TAMs), and the tumor matrix around the TSC niche. The TAMs play a central role in orchestrating neoplastic growth around the TSCs. The lactate-dependent transition from M1 (tumoricidal) macrophages to M2 (immunosuppressive and pro-tumorigenic) phenotype is considered the most critical event of this mechanism. In this chapter, we have attempted to summarize the recent advances in the area of tumor growth associated with hyperglycolysis-inflammation connect in general and on the TAM-mediated endothelial-mesenchymal transition (EMT), required for angiogenesis and metastasis in the growing in vivo tumors in particular. The key hyperglycolytic players focused are hexokinase II, inducible phosphofructokinase 2, pyruvate kinase M2, and M4-lactate dehydrogenase, and those of inflammation are colony-stimulating factor 1 (CSF1) and several other cytokines. The TAM, the programmed cell death-1 ligand (PD-L1), and PD-1-mediated suppression of T cell response against cancer cells have been given special focus. Similarly, the role of REDD1 (regulated in development and DNA damage responses 1), a potent stress response factor, in TAM-mediated metastasis and neovascularization, has been advocated as an evolving concept of TAM-mediated tumorigenesis. In view of the above, we have tried to summarize the current status about whether these key players of hyperglycolysis-inflammation axis could be exploited as targets for restricting tumor growth in vivo. © Springer Nature Singapore Pte Ltd. 2022.PublicationReview Natural products as therapeutic interventions for inflammation-mediated cancer(Springer Science and Business Media B.V., 2025) Srabaita Roy; Ranjit Shaw; Akanksha Pandey; Surendra Kumar TrigunInflammation serves as the body’s immune response mechanism against noxious irritants, ranging from removing factors causing injury to regenerating damaged tissue. Chronic inflammation, in particular, has emerged as a crucial contributor to both the development of cancer and its spread through a variety of mechanisms. This phenomenon is referred to as inflammation-induced tumorigenesis. Differing from other forms of inflammation that typically precede tumor formation, ‘cancer-elicited inflammation (CEI)’ is induced following the initiation of a tumor. Beyond the cell-autonomous effects observed in cancer cells, the activation of several oncogenes, including KRAS and MYC, coupled with the rendering of tumor suppressors, for instance, TP53 inactive, triggers programs at the transcription level that culminate in the formation of a tumor-encouraging microenvironment. This is accomplished by the overproduction of chemokines and pro-inflammatory cytokines, immune cell recruitment, and the initiation of angiogenesis. Although it is critical to comprehend the mechanisms by which inflammation aids in the development of cancer, the impact that tumors themselves have on the immune system must be considered because these effects have significant repercussions for the therapy and prevention of cancer. This comprehensive review primarily centers on various inflammatory pathways that have been influenced by cancer and have, in turn, influenced cancer progression. Additionally, we delve deeply into the intricate mechanisms through which specific natural products exert regulatory control over the complex molecular foundations that drive their robust anti-inflammatory and anti-cancer effects. © The Author(s) 2025.PublicationArticle Pharmaceutical characterization and exploration of Arkeshwara rasa in MDA-MB-231 cells(Elsevier B.V., 2024) Remya Jayakumar; Manoj Kumar Dash; Pankaj Kumar; Shiwakshi Sharma; Saumya Gulati; Akanksha Pandey; Kaushavi Cholke; Zeeshan Fatima; S.K. Trigun; Namrata JoshiBackground: The diverse specificity mode of cancer treatment targets and chemo resistance demands the necessity of drug entities which can address the devastating dynamicity of the disease. Objectives: To check the anti-tumour potential of traditional medicine rich in polyherbal components and metal nanoparticle namely Arkeshwara rasa (AR). Material methods: The AR was prepared in a modified version with reference from Rasaratna Samuchaya and characterized using sophisticated instrumental analysis including XRD, SEM-EDAX, TEM, TGA-DSC, and LC-MS and tested against the MDA-MB-231 cell line to screen cell viability and the cytotoxicity with MTT, SRB and the AO assay. Results: XRD pattern shows cubic tetrahedrite structure with Sb, Cu, S peaks and trace elements like Fe, Mg, etc. The particle size of AR ranges between 20 and 30 nm. The TGA points thermal decomposition at 210 °C and the metal sulphide peaks in DSC. LC-MS analysis reveals the components of the formulation more on the flavonoid portion. The IC50 value of MTT and SRB are 25.28 μg/mL and 31.7 μg/mL respectively. The AO colorimeter substantiated the cell viability and the apoptosis figures of the same cell line. The AR exhibits cytotoxicity and reaffirms the apoptosis fraction with SRB assay. Conclusions: The Hesperidine, Neohesperidin, Rutin components in the phytochemical pool can synergize the anti-tumour potential with either influencing cellular pathways or decreasing chemo resistance to conventional treatment. AR need to be further experimented with reverse transcription, flow cytometry, western blotting, etc. © 2023 The AuthorsPublicationArticle Preliminary data on cytotoxicity and functional group assessment of a herb-mineral combination against colorectal carcinoma cell line(Walter de Gruyter GmbH, 2024) Remya Jayakumar; Manoj Kumar Dash; Saumya Gulati; Akanksha Pandey; Surendra Kumar Trigun; Namrata JoshiObjectives: The invasive screening methods and the late stage diagnosis of colorectal carcinoma (CRC) are contributing for the devastative prognosis. The gradual shift of the disease pattern among younger generations requires the implementation of phytochemicals and traditional medicines. Arkeshwara rasa (AR) is a herb-mineral combination of Tamra bhasma/incinerated copper ashes and Dwigun Kajjali/mercury sulphide levigated with Calotropis procera leaf juice, Plumbago zeylanica root decoction and the decoction of three myrobalans (Terminalia chebula, Terminalia bellerica, Emblica Officinalis decoction)/Triphala decoction. Methods: The SW-480 cell line was checked for the cytotoxicity and the cell viability criteria with MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) assay. The acridine orange/ethidium bromide (AO/EtBr) assay revealed the depth of apoptosis affected cells in the fluorescent images. The FTIR analysis exhibited the graphical spectrum of functional groups within the compound AR. Results: The IC50 from the 10-7 to 10-3 concentrations against SW-480 cells was 40.4μg/mL. The staining of AO/EtBr was performed to visualize live and dead cells and it is evident from the result that number of apoptotic cells increases at increasing concentration of AR. The single bond with stretch vibrations of O-H and N-H are more concentrated in the 2,500-3,200cm-1 and 3,700-4,000cm-1 of the spectra whereas, the finger print region carries the O-H and S=O type peaks. Conclusions: The AR shows strong cyto-toxicity against the SW-480 cells by inducing apoptosis. It also modulates cellular metabolism with the involvement of functional groups which antagonizes the strong acids. Moreover, these effects need to be analyzed further based in the in vivo and various in vitro models. © 2023 Walter de Gruyter GmbH, Berlin/Boston.PublicationArticle Rab11 maintains the undifferentiated state of adult midgut precursors via DPP pathway(Elsevier Inc., 2024) Akanksha Pandey; Jagat Kumar RoyAsymmetric stem cell divisions play instrumental roles in the maintenance, growth and differentiation of organs. Failure of asymmetric stem cell divisions may result in an array of developmental disorders, including cancer. It is well established that the gene, inscuteable, acts as the upstream component of asymmetric cell divisions. In Drosophila larval midgut, a founder adult midgut precursor (AMP) experiences an asymmetric division to instruct its first daughter to become a peripheral cell that serves as a niche where the AMP and its future daughters can remain undifferentiated. The present study demonstrates that inscuteable expressing stem cells require Rab11, a conserved small Ras-like GTPase, for proper proliferation and differentiation. As insc-GAL4 mediated Rab11RNAi in Drosophila larval and adult midguts show the disruption of the niche microenvironment of adult midgut precursors as well as elevated DPP signalling at the larval stage, which is associated with aberrant over-proliferation and early differentiation of larval AMPs and adult intestinal stem cells. The observed connections between Rab11, larval AMP proliferation, niche establishment, and DPP signalling highlight the potential for Rab11 to serve as a key regulatory factor in maintaining tissue homeostasis and balanced cellular growth. © 2024 Elsevier Inc.PublicationArticle Rab11 plays a key role in stellate cell differentiation via non-canonical Notch pathway in Malpighian tubules of Drosophila melanogaster(Elsevier Inc., 2020) Praween Kumar Choubey; Nabarun Nandy; Akanksha Pandey; Jagat Kumar RoyRab11, a member of Rab-GTPase family, and a marker of recycling endosomes has been reported to be involved in the differentiation of various tissues in Drosophila. Here we report a novel role of Rab11 in the differentiation of stellate cells via the non-canonical Notch pathway in Malpighian tubules. During Malpighian tubule development caudal visceral mesodermal cells intercalate into the epithelial tubule of ectodermal origin consisting of principal cells, undergo mesenchymal to epithelial transition and differentiate into star shaped stellate cells in adult Malpighian tubule. Two transcription factors, Teashirt and Cut (antagonistic to each other) are known to be expressed in stellate cells and principal cells, respectively, from early stages of development and serve as markers for these cells. Inhibition of Rab11 function or over-expression of activated Notch in stellate cells resulted in the expression of Cut that leads to down-regulation of Teashirt or vice-versa that leads to hampered differentiation of stellate cells. The stellate cells do not transform to star/bar shaped and remain in mesenchymal state in adult Malpighian tubule. Over-expression of Deltex, which plays important role in non-canonical Notch signaling pathway, shows similar phenotype of stellate cells as seen in individuals with down-regulated Rab11, while down-regulation of Deltex in genetic background of Rab11RNAi rescues Teashirt expression and shape of stellate cells. Our experiments suggest that an inhibition or reduction of Rab11 function in stellate cells results in the faulty recycling of Notch receptors to plasma membrane as they accumulate in early and late endosomes, leading to Deltex mediated non-canonical Notch activation. © 2020 Elsevier Inc.PublicationArticle The insc-GAL4 driver marks distinct cell types in Drosophila midgut(Elsevier Inc., 2024) Akanksha Pandey; Jagat Kumar RoyDrosophila geneticists frequently employ the binary GAL4-UAS system of conditional gene expression to direct expression of the desired transgene in tissues of interest. The inscuteable -GAL4 driver (insc-GAL4) expresses in the type 1 and type 2 neuroblasts of Drosophila larval brain, a frequent target tissue in many investigations. This GAL4 line additionally displayed its expression in the midgut. In this study, we examined the expression of the UAS-mCD8GFP reporter under the command of the insc-GAL4 driver and observed that this driver expresses exclusively to intestinal stem cells (ISCs) of the Drosophila adult midgut as well as adult midgut precursors (AMPs) of the larval midgut besides its expression in larval brain. Additionally, using the G-TRACE method, it was observed that AMPs in the larval midgut consistently expressed insc-GAL4 in real-time, and the lineage expression of this GAL4 was observed in the enterocyte cells. This study reveals for the first time that insc-GAL4 is specific to larval AMPs and adult ISCs of the midgut. © 2024 Elsevier Inc.
