7,819 research outputs found
Panus bambusinus N. Vinjusha & T. K. A. Kumar 2022, comb. nov.
No full textPanus bambusinus (T.K.A. Kumar & Manim.) N. Vinjusha & T.K.A. Kumar comb. nov. MycoBank No: MB 842791 Basionym:— Lentinus bambusinus T.K.A. Kumar & Manim., in Mycotaxon 92: 119 (2005) The species is characterized by graminicolous basidiomata, a dimitic hyphal system, with sparsely branched skeletal hyphae, presence of refractive gloeocystidia, ellipsoid to ovoid basidiospores, and absence of hyphal pegs and skeleto ligative hyphae (Kumar & Manimohan 2005; Vinjusha & Kumar 2021).Published as part of Kumar, T. K. Arun, 2022, Validation of Panus bambusinus and P. roseus (Panaceae, Polyporales), pp. 235-236 in Phytotaxa 533 (4) on page 235, DOI: 10.11646/phytotaxa.533.4.7, http://zenodo.org/record/609165
Panus roseus N. Vinjusha & T. K. A. Kumar 2022, comb. nov.
No full textPanus roseus (Karun., K.D. Hyde & Zhu L. Yang) N. Vinjusha & T.K.A. Kumar comb. nov. MycoBank No: MB 842792 Basionym:— Lentinus roseus Karunarathna, K.D. Hyde & Zhu L. Yang, in Karunarathna, Yang, Zhao, Vellinga, Bahkali, Chukeatirote & Hyde, Mycol. Progr. 10 (4): 392 (2011) Panus roseus is characterized by a relatively small basidiome, with coriaceous, deeply cyathiform, pink-coloured pileus, dimitic hyphal system, with thick-walled unbranched skeletal hyphae, presence of clavate, cheilocystidia and metuloids, and ellipsoid to elongate basidiospores (Karunarathna et al. 2011).Published as part of Kumar, T. K. Arun, 2022, Validation of Panus bambusinus and P. roseus (Panaceae, Polyporales), pp. 235-236 in Phytotaxa 533 (4) on page 235, DOI: 10.11646/phytotaxa.533.4.7, http://zenodo.org/record/609165
Silencing of PTOV1 and PIN1 lead to the G2/M arrest in MDA-MB-231 cells.
No full text(A) Histogram representing the cell cycle distribution of MDA-MB-231 cells transfected with PTOV1 siRNA for 48 hours (left panel) and statistical representation of percentage distribution of the population in each phase (right panel). (B) Histogram representing the cell cycle distribution of MDA-MB-231 cells transfected with PIN1siRNA for 48 hours (left panel) and statistical representation of percentage distribution of the population in each phase (right panel). Data are represented as mean ± SD of three independent experiments. *, *** Significant difference from scramble groups (p < 0.05 & 0.001).</p
MBCD decreased stemness in MDA-MB-231.
No full text(A) Colony formation assay was performed. MDA-MB-231 cells were plated at low density (1000 cells/well) in 6 well plates. After 24 hr, cells were treated with MBCD (1mM). After 5 days, formed colonies were stained with crystal violet. Photos of the wells were taken by a camera (Upper panel of A). Colonies were visualized by inverted bright field microscope. Arrows depict the colonies. (B) Bars represent the average colony count of three independent fields. Value represents mean ± SEM, **p C) Soft agar assay of MDA-MB-231 cells in presence and absence of MBCD (1mM). Day zero and day 9 pictures were shown in the figure. Arrows depict the spheres. (D) Bars showed average of spheroid counts. Value represents mean ± SEM of three independent measurements, **p E) RT-PCR analysis was performed using total RNA and gene specific primers. Decreased levels of stemness markers CD44 and BMI1 were found in MBCD treated cells. GAPDH was measured as loading control. Densitometry analysis was shown in S1C Fig.</p
Evaluation of ROS generation in MDA-MB-231 cells using the fluorescent probe DCF-DA.
No full textA. Qualitative measurement of intracellular ROS levels in MDA-MB-231 cells fluorescence images were taken at 10x magnification. Cells were treated with extracts at 31.25 μg/mL and 250 μg/mL and with positive control (50 μM H2O2) for 24 h. Fluorescence images indicated that methanolic extract induced intracellular ROS generation in MDA-MB-231 cells. B. Quantitative measurement of intracellular ROS levels in MDA-MB-231 cells. Cells were treated with different concentrations of methanolic extract and positive control (50 μM H2O2) for 12 h. Data are means ± SD of triplicate in three independent experiments. * indicates statistically significant difference from corresponding controls (one-way ANOVA, P < 0.05).</p
Influence of metformin on MDA-MB-231 cell viability.
No full text(A) MDA-MB-231 cells were treated with various concentrations of metformin for 24 hrs. MTT assay was performed as an index of cell viability as described in methods. Values represent mean ± SEM of triplicate measurements, **p B) Apoptosis assay was performed as described in methods. Metformin treatment increased the apoptotic cell population as compared to control cells. Here, number of apoptotic cell population was mentioned. (C) RT-PCR analysis was performed using total RNA isolated from metformin (2 mM) treated and untreated cells, and gene specific primers. Decreased levels of anti-apoptotic markers BCL2 and Bcl-xL mRNAs were found in metformin treated cells. Elevated levels of apoptotic markers caspase3 and Bax transcripts were observed in metformin treated cells. (D) Bars showed densitometry analysis (ratio of concerned gene/ GAPDH). * p < .05 vs. control. Values represent mean ± SEM of three replicates.</p
Effect of methanolic extract on MMP in MDA-MB-231 cells using JC-1 fluorescence dye.
No full textA. Methanolic extract induced MMP depolarization in MDA-MB-231 cells. The cells were treated with extracts at 31.25 μg/mL and 250 μg/mL and with positive control (50 μM CCCP) for 12 h. Cells were imaged with an inverted fluorescence microscope (Zeiss Axiovert A) at 40x magnification. The emitted green fluorescence indicates MMP depolarization, which is an early event in apoptosis. B. Relative quantification of MMP (ΔΨm) in MDA-MB-231 cells. Cells were treated with different concentrations of methanolic extract and positive control (50 μM CCCP) for 12 h. Methanolic extract disrupts MMP (ΔΨm). Data are means ± SD of triplicate in three independent experiments. * indicates statistically significant difference from corresponding controls (one-way ANOVA, P < 0.05).</p
Effect of <i>S</i>. <i>ferruginea</i> extracts on colony-forming abilities of MDA-MB-231 cells.
No full text(A). Methanolic (a) and aqueous (b) extracts suppressed colony formation in a dose dependent manner. The methanolic extract inhibited the clonogenicity of MDA-MB-231 cells more effectively than the aqueous extract. (B) Quantitative measurement of colony formation of selected extracts on MDA-MB-231 cells at different concentration (31.25–1000 μg/mL). The colony forming ability of the cells at each dose of the extract is expressed in terms of percent of untreated control cells. Data are means ± SD of triplicate in three independent experiments. * indicates statistically significant difference from their respective untreated control (one-way ANOVA, P < 0.05).</p
Western blot analysis of PARP protein in MDA-MB-231 cells.
No full textMDA-MB-231 cells were treated with S. ferruginea methanolic extract at IC50 for indicated times. Control cells were treated with 0.1% DMSO. β-Actin was used as loading control. The PARP protein (116-kDa) was cleaved into its signature 85-kDa fragment, a marker of apoptosis, after treatment with the methanolic extract. The densitometric-intensity data are presented as means ± SEM of triplicate in three independent experiments. * indicates statistically significant difference from control (one-way ANOVA, P < 0.05).</p
Knockdown of PTOV1 and PIN1 exhibit common phenotypic anti-cancer effects in MDA-MB-231 cells
No full textBackgroundEarlier, we have identified PTOV1 as a novel interactome of PIN1 in PC-3 cells. This study aims to explore the functional similarity and the common role of both genes in breast cancer cell proliferation.MethodsCTG, crystal violet assay, clonogenic assay, wound healing assay, cell cycle analysis, Hoechst staining and ROS measurement were performed to assess cell viability, colony forming potential, cell cycle arrest, nuclear condensation and ROS production after knocking down of PTOV1 and PIN1 by siRNAs in MDA-MB-231 and MCF-7 cells. CO-IP, qPCR and western blot were performedto study interaction, transcriptional and translational regulation of both genes.ResultsKnockdown of PTOV1 and PIN1 inhibited the cell proliferation, colony formation, migration, cell cycle, and induced nuclear condensation as well as ROS production. Interaction of PTOV1 and PIN1 was validated by Co-IP in MDA-MB-231 cells. Genes involved in cell proliferation, migration, cell cycle, and apoptosis were regulated by PIN1 and PTOV1. PTOV1 knockdown inhibited Bcl-2, Bcl-xL and inducedBAX, LC3 and Beclin-1expression. Overexpression of PIN1 increased the expression of PTOV1. Knockdown of both genes inhibited the expression of cyclin D1, c-Myc, and β-catenin.ConclusionsPTOV1 and PIN1 interact and exert oncogenic role in MDA-MB-231 cells by sharing the similar expression profile at transcriptional and translational level which can be a promising hub for therapeutic target.</div
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