Journal: Cell Reports Medicine

Article Title: The SGLT2 inhibitor dapagliflozin ameliorates renal fibrosis in hyperuricemic nephropathy

doi: 10.1016/j.xcrm.2024.101690

Figure Lengend Snippet: Effects of dapagliflozin on renal fibrosis of patients with HN (A and B) Representative images of H&E, Masson staining and quantitation of tubular injury score, and Masson staining-positive area in kidney sections from each patient group. (C) Representative images of αSMA (green), FN1 (red), and LTL (white) immunofluorescent staining and quantitation of αSMA and FN1 fluorescence intensity in kidney sections from each patient group. (D) Representative TEM images of mitochondria and quantitation of aspect ratio, circularity, and roundness in kidney sections from each patient group. Red outlines indicate mitochondria. (E) Representative images of TOM20 (red) and LTL (white) immunofluorescent staining and quantitation of TOM20 fluorescence intensity in kidney sections from each patient group. (F) Schematic diagram of the RNA-seq using kidneys from HN-animals, UA-treated cells. (G and I) Heatmap showing the upregulation of fibrotic pathway and inflammation in kidneys from HN mice (GEO: GSE190205) or UA-treated cells (GEO: GSE198133) versus the control group. (H, J, and K) Representative quantitation of αSMA and FN1 mRNA levels normalized to β-actin in isolated renal tubules, TECs, or HK-2 cells per group. (L) Chemical structure formula of dapagliflozin in 2D and 3D conformer. (M and N) Representative images of H&E, Masson staining and quantitation of tubular injury score, and Masson staining-positive area in kidney sections from each patient group. (O) Renal survival percent (an increase in serum Cr levels to twice the baseline value) (Kaplan-Meier curve) in each patient group over time. Log-rank test p < 0.001. A, adenine; P, potassium oxonate; Dapa, dapagliflozin. control patients ( N = 6), patients with HN ( N = 12), and patients with HN + Dapa ( N = 12); n = 3 cultures per group; ns: not significant ( p > 0.05), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; five visual fields for each section analyzed.

Article Snippet: SGLT2-KO HK2 cell , Cyagen , N/A.

Techniques: Staining, Quantitation Assay, Fluorescence, RNA Sequencing, Control, Isolation

Journal: Cell Reports Medicine

Article Title: The SGLT2 inhibitor dapagliflozin ameliorates renal fibrosis in hyperuricemic nephropathy

doi: 10.1016/j.xcrm.2024.101690

Figure Lengend Snippet: Effects of dapagliflozin or ERRα overexpression in UA-treated TECs and HK-2 cells (A and B) Representative western blots of ERRα, αSMA, and FN1 protein and quantification of protein levels normalized to β-actin in each TEC group. (C) Representative images of ERRα (green) and FN1 (red) immunofluorescent staining and quantitation of fluorescence intensity in each TEC group. (D and E) Representative TEM images of mitochondria and quantitation of inner mitochondrial membrane (IMM)/outer mitochondrial membrane (OMM) ratio, total cristae length/mitochondrial area, and cristae junction/mitochondrial area in each TEC group. Red outlines indicate the zoom area. (F) Representative traces show OCR in each TEC group. (G) Representative quantitation of ATP levels in each TEC group. (H) Representative images of MitoTracker (red) immunofluorescent staining and quantitation of mitochondrial morphology in each TEC group. White outlines indicate the zoom area. (I) Representative images of ROS (green) immunofluorescent staining and quantitation of fluorescence intensity in each TEC group. (J) Diagram of the spatial binding pattern of dapagliflozin and ERRα protein. (K) Dapagliflozin’s bond with ERRα analyzed by surface plasmon resonance (SPR). (L) Dapagliflozin’s bond with ERRα analyzed by microscale thermophoresis (MST). (M and O) Representative images of αSMA (green) and FN1 (red) immunofluorescent staining and quantitation of fluorescence intensity in each TEC and HK-2 cell group. (N, P, and Q) Representative western blots of ERRα, αSMA, and FN1 protein and quantification of protein levels normalized to β-actin in each TEC and HK-2 cell group. (R and S) Representative TEM images of mitochondria and quantitation of IMM/OMM ratio, total cristae length/mitochondrial area, and cristae junction/mitochondrial area in each HK-2 cell group. Red outlines indicate the zoom area and mitochondria. Dapa, dapagliflozin; n = 3 cultures per group; MitoTracker, mitochondrial marker; Hoechst, nucleus marker; ns: not significant ( p > 0.05), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; five visual fields for each section analyzed.

Article Snippet: SGLT2-KO HK2 cell , Cyagen , N/A.

Techniques: Over Expression, Western Blot, Staining, Quantitation Assay, Fluorescence, Membrane, Binding Assay, SPR Assay, Microscale Thermophoresis, Marker

Journal: Cell Reports Medicine

Article Title: The SGLT2 inhibitor dapagliflozin ameliorates renal fibrosis in hyperuricemic nephropathy

doi: 10.1016/j.xcrm.2024.101690

Figure Lengend Snippet: Effects of dapagliflozin in UA-treated SGLT2- or ERRα-KO HK-2 cells (A and H) Diagram of the SGLT2 or ERRα gene KO by CRISPR-Cas9 technology and sequencing identification in HK-2 cells. (B and I) Representative western blots of SGLT2, ERRα, αSMA, and FN1 protein and quantification of ERRα, αSMA, and FN1 protein levels normalized to β-actin in each HK-2 cell group. (C and J) Representative images of ERRα (green) and FN1 (red) immunofluorescent staining and quantitation of fluorescence intensity in each HK-2 cell group. White outlines indicate the zoom area. (D and K) Representative images of ROS (green) immunofluorescent staining and quantitation of fluorescence intensity in each HK-2 cell group. White outlines indicate the zoom area. (E and L) Representative images of MitoTracker (red) immunofluorescent staining and quantitation of mitochondrial morphology in each HK-2 cell group. White outlines indicate the zoom area. (F and M) Representative traces show OCR in each HK-2 cell group. (G and N) Representative quantitation of ATP level in each HK-2 cell group. Dapa, dapagliflozin; n = 3 cultures per group; MitoTracker, mitochondrial marker; Hoechst, nucleus marker; ns: not significant ( p > 0.05), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; five visual fields for each section analyzed.

Article Snippet: SGLT2-KO HK2 cell , Cyagen , N/A.

Techniques: CRISPR, Sequencing, Western Blot, Staining, Quantitation Assay, Fluorescence, Marker

Journal: Cell Reports Medicine

Article Title: The SGLT2 inhibitor dapagliflozin ameliorates renal fibrosis in hyperuricemic nephropathy

doi: 10.1016/j.xcrm.2024.101690

Figure Lengend Snippet: ERRα-OAT1 axis in HK-2 cells (A) Chord plots showing KEGG-enriched items of DEGs from HK-2 cells of the control group versus the si-ERRα group. (B) ChIP-seq analysis: the binding site of OAT1 with ERRα in HK-2 cells. (C) ChIP-qPCR analysis: representative agarose gel image showing OAT1 gene fragments enrichment on ERRα protein. (D) Motif analysis: the complementary sequence of the ERRα-targeted motif. (E) Diagram of the spatial binding pattern of ERRα protein and OAT1 gene. (F and G) Representative quantitation of OAT1 mRNA and protein levels normalized to β-actin, representative western blots of ERRα and OAT1 protein, and quantification of protein levels normalized to β-actin in each TEC and HK-2 cell group. (H) Schematic diagram showing the location of the ERRα-targeted motif (in the OAT1 gene’s promoter region) when inserted upstream of the luciferase gene. Dual-luciferase reporter assay: relative luciferase activity in each group of HK-2 cells. (I and J) Representative western blots of ERRα and OAT1 protein and quantification of protein levels normalized to β-actin in each TEC and HK-2 cell group. n = 3 cultures per group; ns: not significant ( p > 0.05), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: SGLT2-KO HK2 cell , Cyagen , N/A.

Techniques: Control, ChIP-sequencing, Binding Assay, ChIP-qPCR, Agarose Gel Electrophoresis, Sequencing, Quantitation Assay, Western Blot, Luciferase, Reporter Assay, Activity Assay

Journal: Cell Reports Medicine

Article Title: The SGLT2 inhibitor dapagliflozin ameliorates renal fibrosis in hyperuricemic nephropathy

doi: 10.1016/j.xcrm.2024.101690

Figure Lengend Snippet:

Article Snippet: SGLT2-KO HK2 cell , Cyagen , N/A.

Techniques: Virus, Control, Recombinant, SYBR Green Assay, Lysis, CCK-8 Assay, ATP Assay, BIA-KA, cDNA Synthesis, Reporter Gene Assay, Plasmid Preparation, Software, Clinical Proteomics

Journal: bioRxiv

Article Title: Functional regulation of 4D metabolic network between multienzyme glucosome condensates and mitochondria

doi: 10.1101/2022.05.16.491844

Figure Lengend Snippet: (a-c) A representative Hs578T cell showing 3D distribution of glucosomes (PFKL-mEGFP, green) relative to mitochondria (MitoTracker-Red, red) under LLSM imaging. Scale bars in (a) and (c), 5 µm and 1 µm, respectively. (d) Percentages of cells showing decreased, increased, and unchanged amounts of glucosomes at single cell levels in the absence (green) and presence (red) of oligomycin A (10 µM) ( N cells = 145). Error bars indicate standard errors. (e-f) Representative cropped regions of interest in the cytoplasm of a live Hs578T cell showing relative spatial distribution of glucosomes (green) and mitochondria (red) in the absence (e) and presence (f) of oligomycin. Scale bars, 1 µm. (g) Percentages of cells showing decreased, increased, and unchanged amounts of glucosomes at single cell levels in the absence (green) and presence (red) of a PDC inhibitor ((6,8-Bis[(phenylmethyl)thio]octanoic acid (CPI 613), N cells = 74). (h-j) A representative Hs578T cell showing spatial distributions of glucosomes (green) and mitochondria (red) after treatment of shRNA HKII . (i) and (j) show the side and the angled views of (h). Scale bars in (h) and (j), 5 µm and 1 µm, respectively. (k) Percentages of cells showing small-volume glucosomes with (red) and without (green) shRNA HKII treatment. Error bars show standard errors from at least 3 independent experiments.

Article Snippet: Lentiviral pGFP-shHKII vector encoding human shRNA HKII (Cat# TL312415) and non-silencing control pGFP-C-shLenti vector (Cat#: TR30023) were purchased from OriGene Technologies Inc (Rockville, MD, USA).

Techniques: Imaging, shRNA

Journal: bioRxiv

Article Title: Functional regulation of 4D metabolic network between multienzyme glucosome condensates and mitochondria

doi: 10.1101/2022.05.16.491844

Figure Lengend Snippet: (a) A histogram of glucosome populations (%) vs. the nearest edge-to-edge distance between glucosomes and mitochondria ( N glucosomes = 2147). A black solid line shows a double exponential fit for the histogram with a function ( f(d) = f(0) + A 1 e -δ1·d + A 2 e -δ2·d ) where mean distances for two subpopulations are expressed as 1/ δ1 and 1/ δ2 . A white arrow as shown in inset represents an example of the nearest edge-to-edge distance between a mitochondrion and a glucosome. (b) Histograms of glucosome populations (%) as a function of the nearest distance between glucosomes and mitochondria in mitochondria-dense (green) and mitochondria-sparse (red) regions ( N glucosomes = 899). (c-d) Histograms of populations of small-volume (< 90 voxels) and large-volume (≥ 90 voxels) glucosomes vs. the nearest distance between glucosomes and mitochondria only from mitochondria-dense regions in the presence (red) and absence (green) of oligomycin A treatment ( N glucosomes = 964). Error bars show standard errors. (e) Volume percentages (%) occupied by small-volume glucosomes at single cell levels with (red) ( N cells = 7) and without (green) shRNA HKII treatment ( N cells = 8). (f) A histogram of glucosome populations (%) vs. the nearest distance between glucosomes and mitochondria after treatment of shRNA HKII ( N glucosomes = 656). (g-h) Normalized apparent concentrations of PFKL and PKM2 as a function of glucosome volume. Note that the normalized apparent concentrations of PFKL and PKM2 are scaled based on the ratio of their partition coefficients . Statistical analyses were performed using a one-way analysis of variance (ANOVA). Statistical significance is defined as p < 0.05 with a 95 % confidence interval while ‘ns’ refers to not significant. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Error bars indicate standard errors from at least 3 independent experiments.

Article Snippet: Lentiviral pGFP-shHKII vector encoding human shRNA HKII (Cat# TL312415) and non-silencing control pGFP-C-shLenti vector (Cat#: TR30023) were purchased from OriGene Technologies Inc (Rockville, MD, USA).

Techniques: shRNA

Journal: Molecular medicine reports

Article Title: Overexpression of microRNA-125b sensitizes human hepatocellular carcinoma cells to 5-fluorouracil through inhibition of glycolysis by targeting hexokinase II.

doi: 10.3892/mmr.2014.2271

Figure Lengend Snippet: Figure 1. miR-125b acts as a tumor suppressor in human hepatocellular carcinoma (HCC) cells. (A) Expression levels of miR-125b in multiple HCC cell lines compared with the normal human liver cell lines THLE-2 and THLE-3. (B) Expression levels of miR‑125b after transfection with pre‑miR-125b in HepG3 and Huh7 HCC cells. (C) Overexpression of miR-125b suppressed HCC cell growth. Columns, mean of three independent experiments; bars, standard error of the mean. *P<0.05; **P<0.01 vs. control. miR, microRNA; Ctrl, control.

Article Snippet: Overexpression vector containing wild-type HK II (Myc-DDK-tagged; RC209482) was purchased from Origene Technologies, Inc. (Rockville, MD, USA).

Techniques: Expressing, Transfection, Over Expression, Control

Journal: Molecular medicine reports

Article Title: Overexpression of microRNA-125b sensitizes human hepatocellular carcinoma cells to 5-fluorouracil through inhibition of glycolysis by targeting hexokinase II.

doi: 10.3892/mmr.2014.2271

Figure Lengend Snippet: Figure 5. Overexpression of miR-125b in HepG3 cells reduces glucose metabolism. (A) Glucose uptake and (B) lactate production were measured in miR-125b‑overexpressing HepG3 cells compared with the Ctrl group. The relative glucose uptake and lactate production of miR-125 overexpressing cells were normalized to the levels in negative control cells. Columns, mean of three independent experiments; bars, standard error of the mean. *P<0.05 vs. control. Ctrl, control; miR, microRNA.

Article Snippet: Overexpression vector containing wild-type HK II (Myc-DDK-tagged; RC209482) was purchased from Origene Technologies, Inc. (Rockville, MD, USA).

Techniques: Over Expression, Negative Control, Control

Journal: Molecular medicine reports

Article Title: Overexpression of microRNA-125b sensitizes human hepatocellular carcinoma cells to 5-fluorouracil through inhibition of glycolysis by targeting hexokinase II.

doi: 10.3892/mmr.2014.2271

Figure Lengend Snippet: Figure 6. Overexpression of miR-125b in hepatocellular carcinoma cells sensitizes 5-FU‑sensitive and 5‑FU‑resistant cells to 5-FU. (A) Overexpression of miR-125b inhibited HepG3 cell viability. 5‑FU‑sensitive cells were transfected with pre-miR-125b for 48 h, then seeded into 48-well plates and treated with the indicated concentrations of 5-FU followed by measurement of cell viability. (B) HepG3 5-FU‑resistant cells were transfected with negative control and pre-miR-125b for 48 h. The cells were seeded into 48-well plates for 5-FU treatments at the indicated concentrations for 48 h followed by cell viability assays. Columns, mean of three independent experiments; bars, standard error of the mean. *P<0.05; **P<0.01, vs. control. 5-FU, 5-fluorouracil; miR, microRNA.

Article Snippet: Overexpression vector containing wild-type HK II (Myc-DDK-tagged; RC209482) was purchased from Origene Technologies, Inc. (Rockville, MD, USA).

Techniques: Over Expression, Transfection, Negative Control, Control

Journal: Molecular medicine reports

Article Title: Overexpression of microRNA-125b sensitizes human hepatocellular carcinoma cells to 5-fluorouracil through inhibition of glycolysis by targeting hexokinase II.

doi: 10.3892/mmr.2014.2271

Figure Lengend Snippet: Figure 7. Restoration of HK II in miR-125b‑overexpressing cells renders HepG3 cells resistant to 5-FU. (A) HepG3 cells were transfected with 200 nM pre-miR-negative control and pre-miR-125b for 48 h followed by transfection with a vector control and an overexpression vector containing wild‑type HK II for 24 h. Cells were then collected and prepared for western blot analysis using anti‑HK II antibody. β-actin served as a loading control. (B) HepG3 cells were transfected with pre-miR-125b and HK II as described above, then the cells were collected and seeded in 48-well plates for 5-FU treatment at the indicated concentrations for 48 h. Cells were assessed by cell viability assays. Columns, mean of three independent experiments; bars, standard error of the mean. *P<0.05; **P<0.01, vs. control. HK, hexokinase; miR, microRNA, 5-FU, 5-fluorouracil.

Article Snippet: Overexpression vector containing wild-type HK II (Myc-DDK-tagged; RC209482) was purchased from Origene Technologies, Inc. (Rockville, MD, USA).

Techniques: Transfection, Negative Control, Plasmid Preparation, Control, Over Expression, Western Blot

Journal: Frontiers in Oncology

Article Title: HK2 Is a Crucial Downstream Regulator of miR-148a for the Maintenance of Sphere-Forming Property and Cisplatin Resistance in Cervical Cancer Cells

doi: 10.3389/fonc.2021.794015

Figure Lengend Snippet: Overexpression of HK2 Correlates with Poor Prognosis in CC Patients. (A) The expression of HK2 in different types of cancer (Oncomine database). (B) The levels of HK2 in TCGA CC and normal tissues were examined using the UALCAN database. (C) Correlation between HK2 expression and tumor stage in CC patients (UALCAN database). (D) The prognostic value of HK2 in CC patients (KM plotter database). (E) The qRT-PCR analysis of HK2 expression in CC cells and normal ectocervical cell line Ect1/E6E7. *** P < 0.001.

Article Snippet: CC cells transfected with HK2 overexpression vector (OriGene, Rockville, MD) or HK2 shRNA (Santa Cruz Biotechnology; Santa Cruz, CA), were subcutaneously injected into the flank of nude mice under aseptic conditions.

Techniques: Over Expression, Expressing, Quantitative RT-PCR

Journal: Frontiers in Oncology

Article Title: HK2 Is a Crucial Downstream Regulator of miR-148a for the Maintenance of Sphere-Forming Property and Cisplatin Resistance in Cervical Cancer Cells

doi: 10.3389/fonc.2021.794015

Figure Lengend Snippet: HK2 Promotes Sphere Formation and CDDP Resistance in CC Cells. (A) Western blot analysis of HK2 expression in CC cells transfected as indicated. (B) The effect of HK2 expression on the sphere formation was investigated using sphere formation assays. (C) Cell viability assay in response to CDDP treatment was determined using CCK-8 assay. (D) The expression of MDR1, SOX2, and OCT4 in CC cells transfected as indicated was detected by the qRT-PCR assay. (E) HK2 overexpression (or knockdown) decreased (or increased) the sensitivity of CC cells to CDDP in vivo . Tumor volume (left) and weight (right) were examined. *** P < 0.001.

Article Snippet: CC cells transfected with HK2 overexpression vector (OriGene, Rockville, MD) or HK2 shRNA (Santa Cruz Biotechnology; Santa Cruz, CA), were subcutaneously injected into the flank of nude mice under aseptic conditions.

Techniques: Western Blot, Expressing, Transfection, Viability Assay, CCK-8 Assay, Quantitative RT-PCR, Over Expression, Knockdown, In Vivo

Journal: Frontiers in Oncology

Article Title: HK2 Is a Crucial Downstream Regulator of miR-148a for the Maintenance of Sphere-Forming Property and Cisplatin Resistance in Cervical Cancer Cells

doi: 10.3389/fonc.2021.794015

Figure Lengend Snippet: HK2 is negatively regulated by miR-145/148a/497 in CC Cells. (A) Prediction analysis revealed that several miRNAs might regulate HK2 expression. (B) The binding sites of miR-145/148a/497 in the wild-type HK2 3′-UTR were shown. (C) Survival analysis using the KM plotter database was conducted to assess the prognostic value of miR-145/148a/497 in CC patients. (D) The overexpression (or knockdown) of miR-145/148a/497 decreased (or increased) the mRNA expression of HK2 in CC cells. *** P < 0.001.

Article Snippet: CC cells transfected with HK2 overexpression vector (OriGene, Rockville, MD) or HK2 shRNA (Santa Cruz Biotechnology; Santa Cruz, CA), were subcutaneously injected into the flank of nude mice under aseptic conditions.

Techniques: Expressing, Binding Assay, Over Expression, Knockdown

Journal: Frontiers in Oncology

Article Title: HK2 Is a Crucial Downstream Regulator of miR-148a for the Maintenance of Sphere-Forming Property and Cisplatin Resistance in Cervical Cancer Cells

doi: 10.3389/fonc.2021.794015

Figure Lengend Snippet: HK2 is a Direct Target Gene of MiR-145/148a/497 in CC Cells. (A, B) Luciferase reporter assays of CC cells that were co-transfected with indicated miRNA mimics (A) or miRNA inhibitors (B) and luciferase vector containing the wild-type or mutated HK2 3′-UTR. *** P < 0.001.

Article Snippet: CC cells transfected with HK2 overexpression vector (OriGene, Rockville, MD) or HK2 shRNA (Santa Cruz Biotechnology; Santa Cruz, CA), were subcutaneously injected into the flank of nude mice under aseptic conditions.

Techniques: Luciferase, Transfection, Plasmid Preparation

Journal: Frontiers in Oncology

Article Title: HK2 Is a Crucial Downstream Regulator of miR-148a for the Maintenance of Sphere-Forming Property and Cisplatin Resistance in Cervical Cancer Cells

doi: 10.3389/fonc.2021.794015

Figure Lengend Snippet: MiR-148a Inhibits Sphere Formation and CDDP resistance in CC Cells. (A) The effect of miR-148a expression on the sphere formation was investigated using sphere formation assays. (B) After transfection with miR-148a mimic or miR-148a inhibitor, CC cells were treated with CDDP and cell viability was measured using cell viability assay. (C) The qRT-PCR analysis of MDR1 , SOX2 , and OCT4 expression in CC cells transfected as indicated. (D) MiR-148a overexpression (or knockdown) increased (or decreased) the sensitivity of CC cells to CDDP in vivo . *** P < 0.001.

Article Snippet: CC cells transfected with HK2 overexpression vector (OriGene, Rockville, MD) or HK2 shRNA (Santa Cruz Biotechnology; Santa Cruz, CA), were subcutaneously injected into the flank of nude mice under aseptic conditions.

Techniques: Expressing, Transfection, Viability Assay, Quantitative RT-PCR, Over Expression, Knockdown, In Vivo

Journal: Frontiers in Oncology

Article Title: HK2 Is a Crucial Downstream Regulator of miR-148a for the Maintenance of Sphere-Forming Property and Cisplatin Resistance in Cervical Cancer Cells

doi: 10.3389/fonc.2021.794015

Figure Lengend Snippet: The MiR-148a/HK2 Axis Mediates Sphere Formation and CDDP Resistance in CC Cells. (A) Western blot analysis of HK2 expression in CC cells transfected as indicated. (B) Sphere formation of CC cells transfected as indicated. (C) Cell viability of CC cells transfected as indicated in the presence of CDDP was detected by the cell viability assay. *** P < 0.001.

Article Snippet: CC cells transfected with HK2 overexpression vector (OriGene, Rockville, MD) or HK2 shRNA (Santa Cruz Biotechnology; Santa Cruz, CA), were subcutaneously injected into the flank of nude mice under aseptic conditions.

Techniques: Western Blot, Expressing, Transfection, Viability Assay

Journal: Frontiers in Oncology

Article Title: HK2 Is a Crucial Downstream Regulator of miR-148a for the Maintenance of Sphere-Forming Property and Cisplatin Resistance in Cervical Cancer Cells

doi: 10.3389/fonc.2021.794015

Figure Lengend Snippet: Correlation between MiR-145/148a/497 and HK2 Expression in CC Tissues. The expression of miR-145, miR-148a, and miR-497 in CC and adjacent normal tissues was measured using the qRT-PCR assays. *** P < 0.001.

Article Snippet: CC cells transfected with HK2 overexpression vector (OriGene, Rockville, MD) or HK2 shRNA (Santa Cruz Biotechnology; Santa Cruz, CA), were subcutaneously injected into the flank of nude mice under aseptic conditions.

Techniques: Expressing, Quantitative RT-PCR

Journal: Frontiers in Oncology

Article Title: HK2 Is a Crucial Downstream Regulator of miR-148a for the Maintenance of Sphere-Forming Property and Cisplatin Resistance in Cervical Cancer Cells

doi: 10.3389/fonc.2021.794015

Figure Lengend Snippet: A Model Shows the Role of the MiR-148a/HK2 Axis in Regulating Sphere Formation and CDDP Resistance of CC Cells.

Article Snippet: CC cells transfected with HK2 overexpression vector (OriGene, Rockville, MD) or HK2 shRNA (Santa Cruz Biotechnology; Santa Cruz, CA), were subcutaneously injected into the flank of nude mice under aseptic conditions.

Techniques: