Journal: Journal of Nutrition and Metabolism

Article Title: Exploring the Role of Licorice and Its Derivatives in Cell Signaling Pathway NF- κ B and MAPK

doi: 10.1155/2024/9988167

Figure Lengend Snippet: Effect of licorice on MAPK pathway.

Article Snippet: 11. , Oral squamous cell carcinoma (OSCC) generally known as oral cancer caused by tobacco and alcohol , Glycyrrhiza glabra and Glycyrrhiza uralensis , Semilicoisoflavone B (SFB) , Human OSCC cell lines SAS, HSC3M3, OECM-1, and SCC9 , Reduction of MAPK along with Ras/Raf/MEK signaling , [ ] .

Techniques: Activation Assay, Infection, Virus, Phospho-proteomics, Expressing, Inhibition

Journal: BMC Genomic Data

Article Title: Mitochondrial DNA sequences and transcriptomic profiles for elucidating the genetic underpinnings of cisplatin responsiveness in oral squamous cell carcinoma

doi: 10.1186/s12863-022-01062-w

Figure Lengend Snippet: Overview of data files/datasets

Article Snippet: In our previous work [ ], we examined the influence of mtDNA alterations on the cisplatin responsiveness of human OSCC cell lines, SAS and H103, obtained from Japanese Cell Bank Research and European Collection of Authenticated Cell Cultures, respectively.

Techniques: Sequencing, Generated, Variant Assay, Microarray, Gene Expression

Journal: International Journal of Molecular Sciences

Article Title: Role of Clostridium perfringens Enterotoxin on YAP Activation in Colonic Sessile Serrated Adenoma/Polyps with Dysplasia

doi: 10.3390/ijms21113840

Figure Lengend Snippet: Effect of CPE on EMT phenotype in HT29 and HCM116 human colon cancer cells. ( A ) Effect of CPE on cell growth in the two cell lines. ( B , C ) Effect of CPE pretreatment on cell growth. HT29 cells ( B ) and HCT116 cells were treated with CPE of IC5 for 24 h. ( C ). ( D ) Effect of CPE on cell invasion. ( E ) Effect of CPE on protein levels of factors associated with BRAF, Hippo pathway, and CLDN4. ( F ) Effect of CPE on protein levels of factors associated with EMT and stemness. ( G ) BRAF mutation, nuclear YAP and protein levels of factors associated with EMT were examined in 4 CRC cases with or without CPE expression. Error bar, standard deviation from 3 independent trials. CLDN4 M, membranous CLDN4; CLDN4 C, cytosolic CLDN4; EMT, epithelial-mesenchymal-transition; IC, inhibitory concentration.

Article Snippet: HT29 and HCT116 human OSCC cell lines were purchased from Dainihon Pharmaceutical Co. (Tokyo, Japan).

Techniques: Mutagenesis, Expressing, Standard Deviation, Concentration Assay

Journal: Cancer Medicine

Article Title: Development of a complete human anti-human transferrin receptor C antibody as a novel marker of oral dysplasia and oral cancer

doi: 10.1002/cam4.267

Figure Lengend Snippet: DNA copy number analysis of oral dysplasia and oral squamous cell carcinoma (OSCC) showed an amplified genomic region at chromosome 3q. Recurrent genetic changes are depicted according to the copy number analyzer for the GeneChip (CNAG) output of the single-nucleotide polymorphism array analysis of eight oral dysplasia and eight OSCC samples. A summary of all of the identified genetic alteration patterns in the (A) oral dysplasia and (B) OSCC samples is shown. Regions with copy number gains are indicated by red lines and losses are indicated by green lines. Red arrows show the common amplified regions of chromosome 3q in the dysplasia and OSCC samples. (C) A precise genomic map of the amplified regions of 3q. Several genes in the TFRC region were identified in the OSCC expression profiles as being expressed at levels that were more than twofold higher than those in the control oral tissues. (D) Scatter plot of the DNA copy number versus the TFRC mRNA expression rate. Correlations were quantified with Spearman's rank correlation coefficient. TFRC, transferrin receptor C.

Article Snippet: Eight human OSCC cell lines (Ca922, HO-1-u-1, HSC2, HSC3, HSC4, SAS, HSQ89, and Sa-3) were purchased from the RIKEN BioResource Center (Ibaraki, Japan).

Techniques: Amplification, Expressing

Journal: Cancer Medicine

Article Title: Development of a complete human anti-human transferrin receptor C antibody as a novel marker of oral dysplasia and oral cancer

doi: 10.1002/cam4.267

Figure Lengend Snippet: TFRC expression in OSCC. (A) The TFRC mRNA level was examined in five primary oral dysplasia tissues, eight OSCC primary tissues, and eight OSCC cell lines (Ca9-22, Ho1u1, HSC2, HSC3, HSC4, HSQ89, SAS, and Sa-3) by quantitative real-time PCR. mRNA samples from the oral tissues of normal healthy volunteers were used as controls. * P < 0.05, ** P < 0.01. (B) TFRC expression was evaluated in primary OSCC tissues compared with normal oral tissues (right panel) and eight OSCC cell lines compared with control keratinocyte HaCaT cells (left panel) by immunoblotting. (C) TFRC expression was evaluated on OSCC cells and control HaCaT cells by flow cytometry using the anti-TFRC antibody. The cells were stained with the phycoerythrin-labeled anti-TFRC antibody, followed by flow cytometry analysis. The figure shows representative flow cytometry histogram profiles of the control keratinocyte cell line (HaCaT) and seven OSCC cell lines (Ca9-22, HSC2, HSC3, HSC4, SAS HSQ89, SAS, and Sa-3). Open histograms represent cells stained with IgG isotype controls, and filled histograms indicate cells stained with the anti-TFRC antibody. * P < 0.01. OSCC, oral squamous cell carcinoma; TFRC, transferrin receptor C.

Article Snippet: Eight human OSCC cell lines (Ca922, HO-1-u-1, HSC2, HSC3, HSC4, SAS, HSQ89, and Sa-3) were purchased from the RIKEN BioResource Center (Ibaraki, Japan).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Flow Cytometry, Staining, Labeling

Journal: Cancer Medicine

Article Title: Development of a complete human anti-human transferrin receptor C antibody as a novel marker of oral dysplasia and oral cancer

doi: 10.1002/cam4.267

Figure Lengend Snippet: Effects of TFRC knockdown and overexpression on OSCC cell growth. (A) A TFRC expression vector was introduced into HSC4 cells, and cell growth was analyzed by MTT assay. The data are shown as the mean ± SD of triplicate samples. * P < 0.05 versus parental HSC4 cells. The TFRC expression level in parental, mock-, and TFRC-transfected HSC4 cells was determined by FACS (B) analysis and (C) immunoblotting. (D) Retroviral vectors containing TFRC shRNA or mock shRNA (control) were transfected into SAS cells. Forty-eight hours after transfection, the ZsGreen-positive cells were sorted and cell growth was analyzed by MTT assay. The data are shown as the mean ± SD of triplicate samples. * P < 0.05 versus parental SAS cells. OSCC, oral squamous cell carcinoma; TFRC, transferrin receptor C; MTT, methyl thiazolyl tetrazolium.

Article Snippet: Eight human OSCC cell lines (Ca922, HO-1-u-1, HSC2, HSC3, HSC4, SAS, HSQ89, and Sa-3) were purchased from the RIKEN BioResource Center (Ibaraki, Japan).

Techniques: Over Expression, Expressing, Plasmid Preparation, MTT Assay, Transfection, Western Blot, shRNA

Journal: Cancer Medicine

Article Title: Development of a complete human anti-human transferrin receptor C antibody as a novel marker of oral dysplasia and oral cancer

doi: 10.1002/cam4.267

Figure Lengend Snippet: Effects of anti-TFRC antibody treatment on OSCC cells. (A) Cell growth curves of various OSCC cell lines (HSC2, HSC3, HSC4, and SAS) and control HaCaT cells after treatment with the indicated concentration of anti-TFRC antibody. The various cell lines were analyzed by MTT assay. * P < 0.05, ** P < 0.01. (B) The percentages of viable cells at 48 or 72 h after treatment with the indicated concentrations of the anti-TFRC antibody were compared between the OSCC and control HaCaT cells. The experiments were performed in triplicate and repeated independently at least three times. * P < 0.05, ** P < 0.01 versus HaCaT cells. (C) Following anti-TFRC antibody treatment for 72 or 96 h, SAS/OSCC and HSC2/OSCC cells were labeled with Annexin-V and propidium iodide, and the percentage of apoptotic cells was determined by flow cytometry. The experiments were performed in triplicate and repeated independently at least three times. (D) The number of viable SAS and HSC2 cells was determined at the indicated time points after treatment with 1.0 mg/mL of the anti-TFRC antibody or PBS. * P < 0.05, ** P < 0.01. (E) Identification of cleaved caspase-3 (arrowheads) in OSCC cells after anti-TFRC antibody treatment. SAS/OSCC cells were treated with the anti-TFRC antibody (1.0 mg/mL) for 48 h, and immunoblotting analysis was performed with an anti-caspase-3 antibody. The asterisk indicates a nonspecific band. (F) The cell cycle phase distribution was determined for SAS and HSC2/OSCC cells at 48 h after anti-TFRC antibody treatment. The cells were labeled with propidium iodide and analyzed on a FACScan flow cytometer. OSCC, oral squamous cell carcinoma; TFRC, transferrin receptor C; MTT, methyl thiazolyl tetrazolium; PBS, phosphate-buffered saline.

Article Snippet: Eight human OSCC cell lines (Ca922, HO-1-u-1, HSC2, HSC3, HSC4, SAS, HSQ89, and Sa-3) were purchased from the RIKEN BioResource Center (Ibaraki, Japan).

Techniques: Concentration Assay, MTT Assay, Labeling, Flow Cytometry, Western Blot

Journal: Cancer Medicine

Article Title: Development of a complete human anti-human transferrin receptor C antibody as a novel marker of oral dysplasia and oral cancer

doi: 10.1002/cam4.267

Figure Lengend Snippet: The induction of CDC and ADCC activities by anti-TFRC antibody treatment. (A) Anti-TFRC antibody-mediated CDC activity in various OSCC cells. The panel shows the percentage of viable cells. After the cells were incubated with human serum complement and anti-TFRC antibody at concentrations ranging from 0.01 to 10 mg/mL, the extent of cell lysis was measured by LDH release and is shown as the percentage of the value obtained from the untreated cells. The experiments were repeated independently at least three times. (B) Anti-TFRC antibody-mediated ADCC activity in various OSCC cells. ADCC assays were performed with the same series of cells used in (A). After incubating the cells with peripheral blood mononuclear cells from a normal donor and 0.01 to 10 mg/mL of the anti-TFRC antibody, the ADCC activity was measured by LDH release. Two OSCC cell lines (HSC2 and SAS) exhibited dose-dependent effects, whereas two other OSCC lines (HSC3 and HSC4) and control HaCaT cells showed no effects. (C) Anti-TFRC antibody-mediated ADCC activity in HSC4/TFRC cells compared with mock or parental HSC4 cells. (D) Anti-TFRC antibody-mediated ADCC activity in SAS/shTFRC cells compared with sh mock or parental SAS cells. The results are shown as the mean ± the for each sample, and all were independently repeated in triplicate. * P < 0.05, ** P < 0.01. CDC, complement-dependent cytotoxicity; ADCC, antibody-dependent cellular cytotoxicity; OSCC, oral squamous cell carcinoma; TFRC, transferrin receptor C; LDH, lactate dehydrogenase.

Article Snippet: Eight human OSCC cell lines (Ca922, HO-1-u-1, HSC2, HSC3, HSC4, SAS, HSQ89, and Sa-3) were purchased from the RIKEN BioResource Center (Ibaraki, Japan).

Techniques: Activity Assay, Incubation, Lysis

Journal: Cancer Medicine

Article Title: Development of a complete human anti-human transferrin receptor C antibody as a novel marker of oral dysplasia and oral cancer

doi: 10.1002/cam4.267

Figure Lengend Snippet: Anti-TFRC antibody treatment blocks the incorporation of transferrin into OSCC cells. Transferrin uptake in the high-TFRC-expressing SAS and HSC2 cell lines at (A) 24 h and (B) 72 h after anti-TFRC antibody treatment. Transferrin was rapidly internalized after 5 min and continuously internalized up to 60 min in the control cells, but the anti-TFRC antibody-treated cells showed inhibited transferrin incorporation. These experiments were performed with a FACScan flow cytometer, and the quantity of internalized transferrin is represented by the MFI. The left panels show the results for the SAS cells and the right panels show the results for the HSC2 cells. The experiments were performed in triplicate and repeated independently at least three times. * P < 0.05, ** P < 0.01. OSCC, oral squamous cell carcinoma; TFRC, transferrin receptor C; MFI, mean fluorescence intensity.

Article Snippet: Eight human OSCC cell lines (Ca922, HO-1-u-1, HSC2, HSC3, HSC4, SAS, HSQ89, and Sa-3) were purchased from the RIKEN BioResource Center (Ibaraki, Japan).

Techniques: Expressing, Flow Cytometry, Fluorescence

Journal: Cancer Medicine

Article Title: Development of a complete human anti-human transferrin receptor C antibody as a novel marker of oral dysplasia and oral cancer

doi: 10.1002/cam4.267

Figure Lengend Snippet: In vivo antitumor activity of the anti-TFRC antibody against OSCC in subcutaneously xenografted mice. (A) The anti-TFRC antibody reduced tumor growth in Rag-2/Jak3 double-deficient ( Rag-2 −/− Jak3 −/− ) immunodeficient mice that were xenografted with SAS cells. The anti-TFRC antibody was intravenously administered at 15 or 7.5 mg/kg twice per week for 3 weeks (arrowheads). Tumor growth was assessed by measuring the volume of each tumor at twice per week. Each group contained five mice. * P < 0.05, ** P < 0.01. (B) Body weights were measured at each time point. The body weights of the treated mice gradually increased during the treatment. (C) The xenografted mice were sacrificed 29 days after treatment, and the weights of the isolated tumors from each group were directly measured. Two photos show typical cases of mice treated with PBS (left) or 15 mg/kg of the anti-TFRC antibody (right). The right panel shows the comparison of the average tumor weights ± standard errors among the three groups. * P < 0.05, ** P < 0.01. OSCC, oral squamous cell carcinoma; TFRC, transferrin receptor C; PBS, phosphate-buffered saline.

Article Snippet: Eight human OSCC cell lines (Ca922, HO-1-u-1, HSC2, HSC3, HSC4, SAS, HSQ89, and Sa-3) were purchased from the RIKEN BioResource Center (Ibaraki, Japan).

Techniques: In Vivo, Activity Assay, Isolation

Journal: International Journal of Molecular Sciences

Article Title: Malic Enzyme 1 Is Associated with Tumor Budding in Oral Squamous Cell Carcinomas

doi: 10.3390/ijms21197149

Figure Lengend Snippet: Effect of extracellular pH on the epithelial–mesenchymal transition (EMT) phenotype in HSC4 and KON oral squamous cell carcinoma (OSCC) cells. ( A , B ) Effect of the knockdown of ME1 on mRNA expression of EMT-associated genes measured by quantitative PCR ( A ) and extracellular pH ( B ) in HSC4 and KON cells. ( C , D ) Effect of the knockdown of lactate dehydrogenase A (LDHA) on extracellular lactate concentration ( C ) and pH ( D ) in HSC4 and KON cells. ( E ) Effect of medium pH on the EMT phenotype in HSC4 and KON cells. Expression was measured by quantitative PCR. Error bar, standard deviation tested by Student’s t -test in three independent trials. CDH, E-cadherin; CLDN, claudin; HIF, hypoxia-inducible factor; siRNA, small interference RNA; siME, siRNA for ME1; siC, control siRNA; siLDHA, siRNA for LDHA.

Article Snippet: We purchased HSC4 and KON human OSCC cell lines from Dainihon Pharmaceutical Co. (Tokyo, Japan).

Techniques: Knockdown, Expressing, Real-time Polymerase Chain Reaction, Concentration Assay, Standard Deviation, Control

Journal: International Journal of Molecular Sciences

Article Title: Malic Enzyme 1 Is Associated with Tumor Budding in Oral Squamous Cell Carcinomas

doi: 10.3390/ijms21197149

Figure Lengend Snippet: Effect of lactate on the EMT phenotype in HSC4 OSCC cells. ( A – C ) Effect of knockdown of pyruvate dehydrogenase (PDH) or inhibition of PDH kinase by dichloroacetate (DCA) on extracellular lactate ( A ), extracellular pH ( B ), and mRNA expression of EMT-associated genes measured by quantitative PCR ( C ) in HSC4 cells. ( D – F ) Effect of knockdown of monocarbonate transporter (MCT)1 on extracellular lactate ( D ), extracellular pH ( E ), and mRNA expression of EMT-associated genes measured by quantitative PCR ( F ) in HSC4 cells. Error bar, standard deviation tested by Student’s t -test in three independent trials. siPDH, siRNA for PDH; siMCT1, siRNA for MCT1.

Article Snippet: We purchased HSC4 and KON human OSCC cell lines from Dainihon Pharmaceutical Co. (Tokyo, Japan).

Techniques: Knockdown, Inhibition, Expressing, Real-time Polymerase Chain Reaction, Standard Deviation

Journal: International Journal of Molecular Sciences

Article Title: Malic Enzyme 1 Is Associated with Tumor Budding in Oral Squamous Cell Carcinomas

doi: 10.3390/ijms21197149

Figure Lengend Snippet: Effect of hypoxia on EMT and mitochondrial function in HSC4 and KON OSCC cells. ( A ) Effect of CoCl 2 -induced hypoxia on cell proliferation in HSC4 and KON OSCC cells. ( B ) Effect of hypoxia on mRNA expression of MMPs in HSC4 and KON OSCC cells. ( C ) Effect of hypoxia on mRNA expression of EMT-associated genes. ( D – F ) Effect of hypoxia on mitochondrial membrane potential (TMRE assay). ( D ), mitochondrial reactive oxygen species (ROS, DHR assay) ( E ), and extracellular pH ( F ). Inserts in ( D , E ) show fluorescent images. Error bar, standard deviation tested by Student’s t -test in three independent trials. Scale bar, 50 μm. GAPDH, glyceraldehyde 3-phosphate dehydrogenase; TMRE, tetramethylrhodamine ethyl ester; ROS, reactive oxygen species; DHR123, dihydrorhodamine 123.

Article Snippet: We purchased HSC4 and KON human OSCC cell lines from Dainihon Pharmaceutical Co. (Tokyo, Japan).

Techniques: Expressing, Membrane, Standard Deviation

Journal: International Journal of Molecular Sciences

Article Title: Malic Enzyme 1 Is Associated with Tumor Budding in Oral Squamous Cell Carcinomas

doi: 10.3390/ijms21197149

Figure Lengend Snippet: Effect of ME1 and hypoxia on yes-associated protein (YAP) activation in HSC4 OSCC cells. ( A , B ) Effect of knockdown of ME1 on phosphorylation ( A ) and nuclear translocation ( B ) of YAP in HSC4 cells. ( C ) Effect of CoCl 2 -induced hypoxia on nuclear translocation of YAP in HSC4 cells. ( D ) Concentrations of nuclear YAP were measured by ELISA. Tubulin and lamin were examined as loading controls. pYAP, phosphorylated YAP; LATS, large tumor suppressor; pLATS, phosphorylated LATS; siME, siRNA for ME1.

Article Snippet: We purchased HSC4 and KON human OSCC cell lines from Dainihon Pharmaceutical Co. (Tokyo, Japan).

Techniques: Activation Assay, Knockdown, Phospho-proteomics, Translocation Assay, Enzyme-linked Immunosorbent Assay