Browsing by Author "Soni Kumari"

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CUTICLE THICKNESS AND ITS ASSOCIATION WITH INSECTICIDE RESISTANCE IN BACTROCERA CUCURBITAE (DIPTERA : TEPHRITIDAE)
(Connect Journal, 2019) Deepak Verma; Soni Kumari; Dinesh Kumar
Bactrocera cucurbitae is a serious pest of cucurbits. So far, many workers have reported resistance against pyrethroid, spinosad and carbamate in different Bactrocera species. Insects’ cuticle plays key role in the insecticide resistance. Aim of present study was to extend our knowledge about the change in cuticle thickness of Bactrocera cucurbitae with age and its effect on the insecticide resistance. The mean cuticle thickness of ageing insects was 4.63 ± 0.36 μm for day 3, = 6.67 ± 0.13 μm for day 9, 10.36 ± 0.11 μm for 15 day old insects. Parallelly, we isolated the resistant and susceptible population of 10 day old Bactrocera cucurbitae and compared the cuticle thickness. In the present investigation, resistant B. cucurbitae were found to have cuticle thickness 15.84% greater than the susceptible flies. To affirm the role of cuticle thickness in insecticide resistance, we treated thoracic and abdominal segments of Bactrocera cucurbitae with insecticide and noted down the survival percentage. Survival percentage was significantly high in case of thoracic application of deltamethrin than the abdominal application. Higher cuticle thickness is associated with improved insecticide resistance in the same age group of Bactrocera cucurbitae population. However, for ageing insects, it protects the insect to a certain life stage © 2020. All Rights Reserved.
Cyclin D1 and cyclin E2 are differentially expressed in gastric cancer
(Humana Press Inc., 2016) Soni Kumari; Puneet; Shyam Babu Prasad; Suresh Singh Yadav; Mohan Kumar; A. Khanna; V.K. Dixit; Gopal Nath; Sunita Singh; Gopeshwar Narayan
Cell cycle regulators cyclin D1 and cyclin E2 function in G1/S transition by activating downstream cyclin-dependent kinases. Deregulated expression of these cyclins has been reported in various cancers. However, little is known about their clinical significance in gastric carcinoma. We aimed to explore that whether there is differential expression of these cyclins in clinically distinct gastric cancer patients. In this study we recruited a total of 92 subjects including 20 controls and 72 cases of histopathologically proven gastric carcinoma. Expression profiling at transcript level was done by semiquantitative RT-PCR and of protein by immunohistochemistry. Receiver operator characteristics analysis was done for determining diagnostic utility of cyclin D1 and cyclin E2. We demonstrate that cyclins D1 and E2 are frequently overexpressed in early stages of gastric carcinoma. Interestingly, expression of cyclins D1 and E2 significantly correlates with different clinical parameters such as gender, histological type (intestinal and diffuse), tumor location (proximal, middle, and distal), tumor differentiation (differentiated and undifferentiated), tumor invasion (serosal, lymphatic, and venous) and tumor metastasis (lymph node, peritoneal, ascites, and liver). Cyclin D1 has significantly higher sensitivity and specificity as diagnostic biomarker than cyclin E2. Our results suggest that overexpression of cyclin D1 and cyclin E2 is an early event in gastric carcinogenesis. The differential expression of these cyclins may be useful as diagnostic biomarkers for early detection of gastric carcinoma. © 2016, Springer Science+Business Media New York.
Epigenetic Mechanisms and Events in Gastric Cancer-Emerging Novel Biomarkers
(Springer Netherlands, 2018) Puneet; Hasan Raza Kazmi; Soni Kumari; Satendra Tiwari; A. Khanna; Gopeshwar Narayan
Gastric cancer is one of the most common malignancy worldwide. The various genetic and epigenetic events have been found to be associated with its carcinogenesis. The epigenetic is a heritable and transient/reversible change in the gene expression that is not accompanied by modification in the DNA sequence. This event is characterized by the alteration in the promoter CpG island of the gene or histone modification. These events are associated with silencing of critical tumor suppressor gene and activation of oncogenes leading to carcinogenesis. The DNA methylation is a chemical change in the DNA sequence that most commonly occurs at cytosine moiety of CpG dinucleotide and histone, primarily on N- terminal tail that ultimately effect the interaction of DNA with chromatin modifying protein. Hypermethylation of tumor suppressor genes and global hypomethylation of oncogenes are widely studied epigenetic modifications. There are large number of publish reports regarding epigenetic events involving gastric cancer. These changes are potentially useful in identifying markers for early diagnosis and management of this lethal malignancy. Also, role of specific miRNAs and long non coding RNAs in regulation of gene expression is gaining interest and is a matter of further investigation. In this review, we aimed to summarize major epigenetic events (DNA methylation) in gastric cancer along with alteration in miRNAs and long non coding RNAs which plays an important role in pathology of this poorly understood malignancy. © 2018, Arányi Lajos Foundation.
Epigenetic silencing of CXCR4 promotes loss of cell adhesion in cervical cancer
(Hindawi Publishing Corporation, 2014) Suresh Singh Yadav; Shyam Babu Prasad; Mitali Das; Soni Kumari; Lakshmi Kant Pandey; Sunita Singh; Satyajit Pradhan; Gopeshwar Narayan
In the network of chemokine signaling pathways, recent reports have described the SDF-1α/CXCR4 axis and its role in cancer progression and metastasis. Interestingly, we found downregulation of CXCR4 at both transcript and protein level in cervical cancer cell lines and primary tumors. We also found CXCR4 promoter hypermethylation in cervical cancer cell lines and primary biopsy samples. DNA hypomethylating drug 5-AZA-2′-deoxycytidine and histone deacetylase inhibitor Trichostatin A treatments in cell lines reactivate both CXCR4 transcription and protein expression. Cell adhesion assay demonstrated that autocrine SDF-1α promotes the loss of cell adhesion while paracrine SDF-1α predominantly protects the normal cervical cells from loss of cell adhesion. Cervical cancer cell line C-33A having increased expression of CXCR4 after TSA treatment showed increased cell adhesion by paracrine source of SDF-1α in comparison to untreated C-33A. These findings demonstrate the first evidence that epigenetic silencing of CXCR4 makes the cells inefficient to respond to the paracrine source of SDF-1α leading to loss of cell adhesion, one of the key events in metastases and progression of the disease. Our results provide novel insight of SDF-1α/CXCR4 signaling in tumor microenvironment which may be promising to further delineate molecular mechanism of cervical carcinogenesis. © 2014 Suresh Singh Yadav et al.
Expression of Mucoproteins in Gallbladder Cancer
(Springer, 2022) Puneet Kumar; Priyesh Shukla; Soni Kumari; Ruhi Dixit; Gopeshwar Narayan; V.K. Dixit; A.K. Khanna
This study was designed to evaluate the correlation of expression profiles of MUC2, MUC4, and MUC5AC to the clinico-pathological parameters in gallbladder cancer. We recruited biopsies of a total of 60 subjects including 50 primary tumor biopsies from histopathologically proven gallbladder cancer and 10 cases of chronic cholecystitis as control. We have investigated the expression levels of MUC2, MUC4, and MUC5AC by semi-quantitative RT-PCR and immune-histochemistry in gallbladder cancer biopsies, and chronic cholecystitis as a control. Clinical correlation of the differential expression of MUC2, MUC4, and MUC5AC was determined using appropriate statistical methods. Our results demonstrated that MUC2 was significantly (p = 0.004) upregulated in 16%, MUC4 was significantly (p = 0.0004) upregulated in 24%, and MUC5AC was significantly (p = 0.003) upregulated in 32% samples at transcript levels in primary gallbladder cancer biopsies in comparison to the control. Similar to RT-PCR data, MUC2 was significantly (p = 0.001) upregulated in 30%, MUC4 was significantly (p = 0.047) upregulated in 48%, and MUC5AC was significantly (p = 0.002) upregulated in 52% samples at proteome levels in primary gallbladder cancer biopsies in comparison to the control. In conclusion, the MUC2, MUC4, and MUC5AC expression were found to be significantly upregulated in gallbladder cancer group than control. The overexpression of MUC2, MUC4, and MUC5AC suggested their association with gallbladder cancer. © 2021, Association of Surgeons of India.
mRNA Expression Analysis of E-Cadherin, VEGF, and MMPs in Gastric Cancer: a Pilot Study
(Springer, 2021) Puneet Kumar; Arun Sebastian; Khushi Verma; Ruhi Dixit; Soni Kumari; Juhi Singh; Satyendra Kumar Tiwary; Gopeshwar Narayan
Gastric cancer (GC) is a serious fatal cancer on a global scale because of its presentation at advanced stage. The expressions of vascular endothelial growth factor (VEGF), E-cadherin, and matrix metalloproteinases (MMPs) in other cancers have been reported. However, its expression and underlying mechanisms are little known in gastric cancer in Indian context. In this study, we detected mRNA expression of VEGF, E-cadherin, and MMPs (MMP-1, MMP-2, and MMP-9) in 73 gastric cancer tissues and 27 normal controls by reverse-transcriptase polymerase chain reaction (RT-PCR). Receiver operator characteristics analysis was done for determining the diagnostic utility of VEGF, MMPs and E-cadherin with respect to the sensitivity and specificity. The association of VEGF, MMPs, and E-cadherin expression with the clinicopathological characteristics and the prognosis was subsequently analyzed. The mRNA expression results showed that E-cadherin was significantly downregulated in 47.9% of GC in comparison to control. There was no change in VEGF expression observed in 90.4% GC cases. MMP-1, MMP-2, and MMP-9 were overexpressed in 13.7%, 28.8%, and 11% of GC, respectively, with significant change in MMP-2 (p ≤ 0.0001) and MMP-9 (p = 0.027) in comparison to control. Our results strengthen the necessity of more studies to elucidate the prophetic role of these genes in the development of gastric cancer. © 2020, Indian Association of Surgical Oncology.
Peptidoglycan and Lipoteichoic Acid Induces Differential mRNA Response of Immune-Related Genes in PBMC of Crossbred, Tharparkar Cattle and Murrah Buffalo
(Taylor and Francis Inc., 2019) Sourabh Sulabh; Manjit Panigrahi; Sheikh Firdous Ahmad; Rajat Varshney; Ankita Verma; Naseer Ahmad Baba; Satish Kumar; Soni Kumari; Anuj Chauhan; Pushpendra Kumar; Bharat Bhushan
Subclinical mastitis, generally caused by Staphylococcus aureus, has a global economic impact all over the world. Hence, it needs to be resolved on higher priority which may be attained via. selection of mastitis resistant animals or inclusion of mastitis resistant trait into herd apart from management care. Diverse hosts with various genetic make-ups encounter pathogens in a diverse manner which in turn leads to contradicting outcome of the disease. Identification of species-wise or breed-wise differential expressed genes in response to S. aureus through relative evaluation of transcripts may be useful for judging the immuno-competency of a species or breed toward mastitis. The present study was undertaken to examine the stimulant effect of S. aureus peptidoglycan (PGN) and lipoteichoic acid (LTA) on Peripheral blood mononuclear cells (PBMC) harvested from blood samples of crossbred cattle, Tharparkar cattle, and Murrah buffaloes. After 6 h of in vitro stimulation qRT-PCR was used to measure the relative mRNA expression of TLR-2, TNF-α, IL-8, IFN-γ and IL-10 genes in stimulated and un-stimulated PBMC. The selected genes revealed significant differences in the pattern of immune response among crossbred cattle, Tharparkar cattle and Murrah buffalo in spite of the same stimulant dose. © 2018, © 2018 Taylor & Francis.
PI3K/AKT pathway-mediated regulation of p27Kip1 is associated with cell cycle arrest and apoptosis in cervical cancer
(Kluwer Academic Publishers, 2015) Shyam Babu Prasad; Suresh Singh Yadav; Mitali Das; Arusha Modi; Soni Kumari; Lakshmi Kant Pandey; Sunita Singh; Satyajit Pradhan; Gopeshwar Narayan
Background: The cyclin-dependent kinase inhibitor p27Kip1 is known to act as a putative tumor suppressor in several human cancers, including cervical cancer. Down-regulation of p27Kip1 may occur either through transcription inhibition or through phosphorylation-dependent proteolytic degradation. As yet, the mechanism underlying p27Kip1 down-regulation and its putative downstream effects on cervical cancer development are poorly understood. Here we assessed the expression and sub-cellular localization of p27Kip1 and its effects on proliferation, cell cycle progression and (inhibition of) apoptosis in cervical cancer cells. Methods: Primary cervical cancer samples (n = 70), normal cervical tissue samples (n = 30) and cervical cancer-derived cell lines (n = 8) were used to assess the expression of p27Kip1 and AKT1 by RT-PCR, Western blotting and immunohistochemistry, respectively. The effects of the PI3K inhibitor LY294004 and the proteasome inhibitor MG132 on cervical cancer cell proliferation were investigated using a MTT assay. Apoptosis and cell cycle analyses were carried out using flow cytometry, and sub-cellular p27Kip1 localization analyses were carried out using immunofluorescence assays. Results: We observed p27Kip1 down-regulation (p = 0.045) and AKT1 up-regulation (p = 0.046) in both the primary cervical cancer samples and the cervical cancer-derived cell lines, compared to the normal cervical tissue samples tested. Treatment of cervical cancer-derived cell lines with the PI3K inhibitor LY294002 resulted in a reduced AKT1 activity. We also observed a dose-dependent inhibition of cell viability after treatment of these cell lines with the proteasome inhibitor MG132. Treatment of the cells with LY294002 resulted in a G1 cell cycle arrest, a nuclear expression of p27Kip1, and a cytoplasmic p27Kip1 accumulation after subsequent treatment with MG132. Additionally, we found that the synergistic effect of MG132 and LY294002 resulted in a sub-G1 cell cycle arrest and apoptosis induction through poly (ADP-ribose) polymerase (PARP) cleavage. Conclusion: Our data suggest that p27Kip1 down-regulation in cervical cancer cells is primarily regulated through PI3K/AKT-mediated proteasomal degradation. The observed synergistic effect of the MG132 and LY294002 inhibitors may form a basis for the design of novel cervical cancer therapies. © 2015, International Society for Cellular Oncology.
Synthesis, characterization, and biological applications of zinc(ii) complexes of the methylthiosalicylate ligand
(Royal Society of Chemistry, 2024) Rajesh Pratap; Soni Kumari; Nishtha Chaturvedi; Rajnikant Mishra; Subrato Bhattacharya
A series of Zn(ii) complexes, [Zn(MTS)2(TMEDA)] (1), [Zn(MTS)2(2,2′-bipy.)] (2), [Zn(MTS)2(1,10-phen.)] (3) and [Zn(MTS)2(4,4-bipy.)2]n (4), where MTS = methylthiosalicylate, TMEDA = tetramethyl ethylenediamine, bipy. = bipyridyl, and phen. = phenanthroline, have been synthesized and characterized by single crystal X-ray analysis and other spectroscopic techniques. The geometry of complex 3 is distorted square pyramidal around the Zn center, while complex 2 has distorted trigonal bipyramidal geometry. Complexes 1 and 4 show distorted tetrahedral geometry, of which complex 4 has a zig-zag polymeric structure. Due to differences in geometries, these Zn complexes are expected to exhibit differences in their biological activities. We have carried out studies on the DNA and protein binding, anticancer activity and cytotoxicity of these complexes. The anticancer activities were cell-line dependent; however, complex 4 was found to be the most active complex. © 2024 The Royal Society of Chemistry.