immortalized human ovarian surface epithelial cell line hose Search Results


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ScienCell human ose cells (hosepics)
Human Ose Cells (Hosepics), supplied by ScienCell, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ScienCell normal human ovarian surface epithelial (hose) cells
Knockdown of HOXA11 antisense ( HOXA11as ) inhibits serous ovarian cancer cell proliferation. (A) Expression of HOXA11as in human ovarian surface <t>epithelial</t> cell line <t>(HOSE)</t> and six ovarian cancer cell lines determined by quantitative real time polymerase chain reaction (qRT-PCR). (B) Knockdown efficiency was determined by qRT-PCR analysis in OVCA429 and SKOV3 cells. Cells were transfected with HOXA11as -specific siRNA (siHOXA11as) and negative control siRNA (siNC). (C, D) Knockdown of HOXA11as significantly reduced cell proliferation in OVCA429 and SKOV3 cells as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Bars indicate mean±standard deviation of three independent experiments performed in triplicate. * p < 0.05 vs. siNC. siHOXA11as, HOXA11as -specific siRNA.
Normal Human Ovarian Surface Epithelial (Hose) Cells, supplied by ScienCell, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ovcar3  (ATCC)
99
ATCC ovcar3
Knockdown of HOXA11 antisense ( HOXA11as ) inhibits serous ovarian cancer cell proliferation. (A) Expression of HOXA11as in human ovarian surface <t>epithelial</t> cell line <t>(HOSE)</t> and six ovarian cancer cell lines determined by quantitative real time polymerase chain reaction (qRT-PCR). (B) Knockdown efficiency was determined by qRT-PCR analysis in OVCA429 and SKOV3 cells. Cells were transfected with HOXA11as -specific siRNA (siHOXA11as) and negative control siRNA (siNC). (C, D) Knockdown of HOXA11as significantly reduced cell proliferation in OVCA429 and SKOV3 cells as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Bars indicate mean±standard deviation of three independent experiments performed in triplicate. * p < 0.05 vs. siNC. siHOXA11as, HOXA11as -specific siRNA.
Ovcar3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC human ovarian epithelial cell line hosepic
LINC00673 promoted the migration and invasion of EOC cells. Notes: ( A ) Relative LINC00673 expression in EOC cell lines compared to <t>HOSEpiC.</t> ( B ) Knockdown of LINC00673 by siRNAs in OVCAR3 and HO8910. ( C and D ) LINC00673 silencing inhibited the migration ( C ) and invasion ( D ) of OVCAR3 and HO8910 cells. ( E ) Overexpression of LINC00673 promoted the migration and invasion of A2780 cells. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. Abbreviations: EOC, <t>epithelial</t> ovarian cancer; NC, LINC00673-negative control lentivirus cells; OE, LINC00673-overexpression lentivirus cells; Vector, LINC00673-vector lentivirus cells.
Human Ovarian Epithelial Cell Line Hosepic, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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China Center for Type Culture Collection human ovarian epithelial cell line (t80 cells)
LINC00673 promoted the migration and invasion of EOC cells. Notes: ( A ) Relative LINC00673 expression in EOC cell lines compared to <t>HOSEpiC.</t> ( B ) Knockdown of LINC00673 by siRNAs in OVCAR3 and HO8910. ( C and D ) LINC00673 silencing inhibited the migration ( C ) and invasion ( D ) of OVCAR3 and HO8910 cells. ( E ) Overexpression of LINC00673 promoted the migration and invasion of A2780 cells. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. Abbreviations: EOC, <t>epithelial</t> ovarian cancer; NC, LINC00673-negative control lentivirus cells; OE, LINC00673-overexpression lentivirus cells; Vector, LINC00673-vector lentivirus cells.
Human Ovarian Epithelial Cell Line (T80 Cells), supplied by China Center for Type Culture Collection, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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European Collection of Authenticated Cell Cultures a2780 human ovarian carcinoma cell line
Dependence of human ovarian <t>A2780</t> (top) and colon HT-29 (bottom) cancer cell viability on different concentrations (shown on a logarithmic scale) of L 1–4 2 Ti, following a 3 day incubation period as analyzed by the MTT assay. Cisplatin IC 50 = 1.6 ± 0.4 μM for A2780 and IC 50 = 25 ± 4 μM for HT-29. H 2 L 1–4 = 1.9 ± 0.7, 1.5 ± 0.1, 1.4 ± 0.6, 7.4 ± 1.5 μM for A2780 and IC 50 = 1.3 ± 0.4, 10 ± 3, 10 ± 3, 26.9 ± 6.2 μM for HT-29 (see maximal inhibition values in Table S1 ). Relative IC 50 values were calculated by nonlinear regression of a variable slope model by GraphPad Prism 5.04 software ([top + bottom plateaus]/2).
A2780 Human Ovarian Carcinoma Cell Line, supplied by European Collection of Authenticated Cell Cultures, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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iCell Bioscience Inc human ovarian surface epithelial cells (hosepic)
Dependence of human ovarian <t>A2780</t> (top) and colon HT-29 (bottom) cancer cell viability on different concentrations (shown on a logarithmic scale) of L 1–4 2 Ti, following a 3 day incubation period as analyzed by the MTT assay. Cisplatin IC 50 = 1.6 ± 0.4 μM for A2780 and IC 50 = 25 ± 4 μM for HT-29. H 2 L 1–4 = 1.9 ± 0.7, 1.5 ± 0.1, 1.4 ± 0.6, 7.4 ± 1.5 μM for A2780 and IC 50 = 1.3 ± 0.4, 10 ± 3, 10 ± 3, 26.9 ± 6.2 μM for HT-29 (see maximal inhibition values in Table S1 ). Relative IC 50 values were calculated by nonlinear regression of a variable slope model by GraphPad Prism 5.04 software ([top + bottom plateaus]/2).
Human Ovarian Surface Epithelial Cells (Hosepic), supplied by iCell Bioscience Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC hamster epithelial cell line cho k1
Dependence of human ovarian <t>A2780</t> (top) and colon HT-29 (bottom) cancer cell viability on different concentrations (shown on a logarithmic scale) of L 1–4 2 Ti, following a 3 day incubation period as analyzed by the MTT assay. Cisplatin IC 50 = 1.6 ± 0.4 μM for A2780 and IC 50 = 25 ± 4 μM for HT-29. H 2 L 1–4 = 1.9 ± 0.7, 1.5 ± 0.1, 1.4 ± 0.6, 7.4 ± 1.5 μM for A2780 and IC 50 = 1.3 ± 0.4, 10 ± 3, 10 ± 3, 26.9 ± 6.2 μM for HT-29 (see maximal inhibition values in Table S1 ). Relative IC 50 values were calculated by nonlinear regression of a variable slope model by GraphPad Prism 5.04 software ([top + bottom plateaus]/2).
Hamster Epithelial Cell Line Cho K1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC ovarian carcinoma cell line designated caov3
Figure 3 Antitumor ecacy of various doses of rhuMAb HER-2 on human <t>CAOV3</t> ovarian tumor xenografts in athymic mice. CAOV3 cells were engineered for overexpression of HER-2 receptor as described in Materials and methods. After 7 days, treatments were instituted with human IgG1 at 100 mg/kg (Group A); murine monoclonal antibody 4D5 at 25 mg/kg (Group B); or rhuMAb HER-2 at 3 mg/kg (Group C), 10 mg/kg (Group D), 30 mg/kg (Group E) or 100 mg/kg (Group F). The antitumor eect of the several doses of rhuMAb HER-2 was compared to that of control human IgG1 and 4D5 treatments over 21 days. Inhibition of tumor growth at day 21 relative to control IgG1 was observed at all doses of rhuMAb HER-2 tested, but only reached statistical signi®cance at the highest dose of rhuMAb HER-2 where a tenfold decrease in tumor size compared to control was found (P50.001). Animal weights on days 1 and 21 were not signi®cantly dierent (data not shown)
Ovarian Carcinoma Cell Line Designated Caov3, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC ovarian breast cancer cell line t 47d
Figure 3 Antitumor ecacy of various doses of rhuMAb HER-2 on human <t>CAOV3</t> ovarian tumor xenografts in athymic mice. CAOV3 cells were engineered for overexpression of HER-2 receptor as described in Materials and methods. After 7 days, treatments were instituted with human IgG1 at 100 mg/kg (Group A); murine monoclonal antibody 4D5 at 25 mg/kg (Group B); or rhuMAb HER-2 at 3 mg/kg (Group C), 10 mg/kg (Group D), 30 mg/kg (Group E) or 100 mg/kg (Group F). The antitumor eect of the several doses of rhuMAb HER-2 was compared to that of control human IgG1 and 4D5 treatments over 21 days. Inhibition of tumor growth at day 21 relative to control IgG1 was observed at all doses of rhuMAb HER-2 tested, but only reached statistical signi®cance at the highest dose of rhuMAb HER-2 where a tenfold decrease in tumor size compared to control was found (P50.001). Animal weights on days 1 and 21 were not signi®cantly dierent (data not shown)
Ovarian Breast Cancer Cell Line T 47d, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC epithelial ovarian cancer eoc cells
(A) Compared to the IOSE cells, the expression of miR-373 was significantly down-regulated in all four <t>EOC</t> cell lines. The expression of miR-373 was the lowest in <t>SKOV3</t> cells. EOC, <t>epithelial</t> ovarian cancer; IOSE, immortalized nontumorigenic human ovarian surface epithelial; * p < 0.05 and ** p < 0.01. (B) SKOV3 cells express high level of miR-373 after transfection with pMSCV-miR-373 compared to the mock control, *** p < 0.001. (C) The effect of miR-373 on morphological changes of SKOV3 cells. More rounded epithelial-like morphology was observed in the miR-373-transfected-SKOV3 cells (bottom), while spindle-shaped mesenchymal-like morphology was observed in the mock control cells (top). (D) E-cadherin (epithelial marker) augmentation and N-cadherin (mesenchymal marker) reduction in SKOV3 after the expression of miR-373. (E-F) Transwell invasion and migration assays of SKOV3 cells expressing miR-373 or mock control. Representative images (×100) are shown on the left and the quantification of five randomly selected fields is shown on the right. The invasive and migratory potential of miR-373 - expressing cells showed a strong reduction compared with mock controls. (G) Decreased cellular migration in miR-373-transfected SKOV3 cells was confirmed by wound scratch assay. (H-I) Representative bioluminescent images of disseminated tumor in nude mice i.p. injected with SKOV3 luc -pMSCV-miR-373 cells (bottom) and SKOV3 luc -pMSCV-NC cells (top), respectively. (J) The anatomical location of metastatic tumors upon macroscopic examination reflected bioluminescence and the number of metastatic tumor between two groups was significantly different, ** p < 0.01.
Epithelial Ovarian Cancer Eoc Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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99
ATCC human neoplastic cell lines
(A) Compared to the IOSE cells, the expression of miR-373 was significantly down-regulated in all four <t>EOC</t> cell lines. The expression of miR-373 was the lowest in <t>SKOV3</t> cells. EOC, <t>epithelial</t> ovarian cancer; IOSE, immortalized nontumorigenic human ovarian surface epithelial; * p < 0.05 and ** p < 0.01. (B) SKOV3 cells express high level of miR-373 after transfection with pMSCV-miR-373 compared to the mock control, *** p < 0.001. (C) The effect of miR-373 on morphological changes of SKOV3 cells. More rounded epithelial-like morphology was observed in the miR-373-transfected-SKOV3 cells (bottom), while spindle-shaped mesenchymal-like morphology was observed in the mock control cells (top). (D) E-cadherin (epithelial marker) augmentation and N-cadherin (mesenchymal marker) reduction in SKOV3 after the expression of miR-373. (E-F) Transwell invasion and migration assays of SKOV3 cells expressing miR-373 or mock control. Representative images (×100) are shown on the left and the quantification of five randomly selected fields is shown on the right. The invasive and migratory potential of miR-373 - expressing cells showed a strong reduction compared with mock controls. (G) Decreased cellular migration in miR-373-transfected SKOV3 cells was confirmed by wound scratch assay. (H-I) Representative bioluminescent images of disseminated tumor in nude mice i.p. injected with SKOV3 luc -pMSCV-miR-373 cells (bottom) and SKOV3 luc -pMSCV-NC cells (top), respectively. (J) The anatomical location of metastatic tumors upon macroscopic examination reflected bioluminescence and the number of metastatic tumor between two groups was significantly different, ** p < 0.01.
Human Neoplastic Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Knockdown of HOXA11 antisense ( HOXA11as ) inhibits serous ovarian cancer cell proliferation. (A) Expression of HOXA11as in human ovarian surface epithelial cell line (HOSE) and six ovarian cancer cell lines determined by quantitative real time polymerase chain reaction (qRT-PCR). (B) Knockdown efficiency was determined by qRT-PCR analysis in OVCA429 and SKOV3 cells. Cells were transfected with HOXA11as -specific siRNA (siHOXA11as) and negative control siRNA (siNC). (C, D) Knockdown of HOXA11as significantly reduced cell proliferation in OVCA429 and SKOV3 cells as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Bars indicate mean±standard deviation of three independent experiments performed in triplicate. * p < 0.05 vs. siNC. siHOXA11as, HOXA11as -specific siRNA.

Journal: Cancer Research and Treatment : Official Journal of Korean Cancer Association

Article Title: Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer

doi: 10.4143/crt.2016.263

Figure Lengend Snippet: Knockdown of HOXA11 antisense ( HOXA11as ) inhibits serous ovarian cancer cell proliferation. (A) Expression of HOXA11as in human ovarian surface epithelial cell line (HOSE) and six ovarian cancer cell lines determined by quantitative real time polymerase chain reaction (qRT-PCR). (B) Knockdown efficiency was determined by qRT-PCR analysis in OVCA429 and SKOV3 cells. Cells were transfected with HOXA11as -specific siRNA (siHOXA11as) and negative control siRNA (siNC). (C, D) Knockdown of HOXA11as significantly reduced cell proliferation in OVCA429 and SKOV3 cells as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Bars indicate mean±standard deviation of three independent experiments performed in triplicate. * p < 0.05 vs. siNC. siHOXA11as, HOXA11as -specific siRNA.

Article Snippet: Normal human ovarian surface epithelial (HOSE) cells were purchased from ScienCell Research Laboratories (San Diego, CA).

Techniques: Knockdown, Expressing, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Transfection, Negative Control, MTT Assay, Standard Deviation

LINC00673 promoted the migration and invasion of EOC cells. Notes: ( A ) Relative LINC00673 expression in EOC cell lines compared to HOSEpiC. ( B ) Knockdown of LINC00673 by siRNAs in OVCAR3 and HO8910. ( C and D ) LINC00673 silencing inhibited the migration ( C ) and invasion ( D ) of OVCAR3 and HO8910 cells. ( E ) Overexpression of LINC00673 promoted the migration and invasion of A2780 cells. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. Abbreviations: EOC, epithelial ovarian cancer; NC, LINC00673-negative control lentivirus cells; OE, LINC00673-overexpression lentivirus cells; Vector, LINC00673-vector lentivirus cells.

Journal: OncoTargets and therapy

Article Title: Long noncoding RNA LINC00673 promotes the proliferation and metastasis of epithelial ovarian cancer by associating with opioid growth factor receptor

doi: 10.2147/OTT.S209784

Figure Lengend Snippet: LINC00673 promoted the migration and invasion of EOC cells. Notes: ( A ) Relative LINC00673 expression in EOC cell lines compared to HOSEpiC. ( B ) Knockdown of LINC00673 by siRNAs in OVCAR3 and HO8910. ( C and D ) LINC00673 silencing inhibited the migration ( C ) and invasion ( D ) of OVCAR3 and HO8910 cells. ( E ) Overexpression of LINC00673 promoted the migration and invasion of A2780 cells. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. Abbreviations: EOC, epithelial ovarian cancer; NC, LINC00673-negative control lentivirus cells; OE, LINC00673-overexpression lentivirus cells; Vector, LINC00673-vector lentivirus cells.

Article Snippet: EOC cell lines (HO8910, OVCAR3, A2780, and ES2) and a normal human ovarian epithelial cell line (HOSEpiC) were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Migration, Expressing, Knockdown, Over Expression, Negative Control, Plasmid Preparation

Dependence of human ovarian A2780 (top) and colon HT-29 (bottom) cancer cell viability on different concentrations (shown on a logarithmic scale) of L 1–4 2 Ti, following a 3 day incubation period as analyzed by the MTT assay. Cisplatin IC 50 = 1.6 ± 0.4 μM for A2780 and IC 50 = 25 ± 4 μM for HT-29. H 2 L 1–4 = 1.9 ± 0.7, 1.5 ± 0.1, 1.4 ± 0.6, 7.4 ± 1.5 μM for A2780 and IC 50 = 1.3 ± 0.4, 10 ± 3, 10 ± 3, 26.9 ± 6.2 μM for HT-29 (see maximal inhibition values in Table S1 ). Relative IC 50 values were calculated by nonlinear regression of a variable slope model by GraphPad Prism 5.04 software ([top + bottom plateaus]/2).

Journal: Inorganic Chemistry

Article Title: Hydrolytically Stable and Cytotoxic [ONO N ] 2 Ti(IV)-Type Octahedral Complexes

doi: 10.1021/acs.inorgchem.2c02737

Figure Lengend Snippet: Dependence of human ovarian A2780 (top) and colon HT-29 (bottom) cancer cell viability on different concentrations (shown on a logarithmic scale) of L 1–4 2 Ti, following a 3 day incubation period as analyzed by the MTT assay. Cisplatin IC 50 = 1.6 ± 0.4 μM for A2780 and IC 50 = 25 ± 4 μM for HT-29. H 2 L 1–4 = 1.9 ± 0.7, 1.5 ± 0.1, 1.4 ± 0.6, 7.4 ± 1.5 μM for A2780 and IC 50 = 1.3 ± 0.4, 10 ± 3, 10 ± 3, 26.9 ± 6.2 μM for HT-29 (see maximal inhibition values in Table S1 ). Relative IC 50 values were calculated by nonlinear regression of a variable slope model by GraphPad Prism 5.04 software ([top + bottom plateaus]/2).

Article Snippet: The cytotoxicity of Ti(IV) complexes was tested on A2780 human ovarian carcinoma cell line (European Collection of Authenticated Cell Cultures) and HT-29 human colorectal adenocarcinoma cell line (American Type Culture Collection).

Techniques: Incubation, MTT Assay, Inhibition, Software

Figure 3 Antitumor ecacy of various doses of rhuMAb HER-2 on human CAOV3 ovarian tumor xenografts in athymic mice. CAOV3 cells were engineered for overexpression of HER-2 receptor as described in Materials and methods. After 7 days, treatments were instituted with human IgG1 at 100 mg/kg (Group A); murine monoclonal antibody 4D5 at 25 mg/kg (Group B); or rhuMAb HER-2 at 3 mg/kg (Group C), 10 mg/kg (Group D), 30 mg/kg (Group E) or 100 mg/kg (Group F). The antitumor eect of the several doses of rhuMAb HER-2 was compared to that of control human IgG1 and 4D5 treatments over 21 days. Inhibition of tumor growth at day 21 relative to control IgG1 was observed at all doses of rhuMAb HER-2 tested, but only reached statistical signi®cance at the highest dose of rhuMAb HER-2 where a tenfold decrease in tumor size compared to control was found (P50.001). Animal weights on days 1 and 21 were not signi®cantly dierent (data not shown)

Journal: Oncogene

Article Title: Remission of human breast cancer xenografts on therapy with humanized monoclonal antibody to HER-2 receptor and DNA-reactive drugs.

doi: 10.1038/sj.onc.1202132

Figure Lengend Snippet: Figure 3 Antitumor ecacy of various doses of rhuMAb HER-2 on human CAOV3 ovarian tumor xenografts in athymic mice. CAOV3 cells were engineered for overexpression of HER-2 receptor as described in Materials and methods. After 7 days, treatments were instituted with human IgG1 at 100 mg/kg (Group A); murine monoclonal antibody 4D5 at 25 mg/kg (Group B); or rhuMAb HER-2 at 3 mg/kg (Group C), 10 mg/kg (Group D), 30 mg/kg (Group E) or 100 mg/kg (Group F). The antitumor eect of the several doses of rhuMAb HER-2 was compared to that of control human IgG1 and 4D5 treatments over 21 days. Inhibition of tumor growth at day 21 relative to control IgG1 was observed at all doses of rhuMAb HER-2 tested, but only reached statistical signi®cance at the highest dose of rhuMAb HER-2 where a tenfold decrease in tumor size compared to control was found (P50.001). Animal weights on days 1 and 21 were not signi®cantly dierent (data not shown)

Article Snippet: Cell lines and cell culture The well-characterized human breast carcinoma cell line, MCF-7, and the human ovarian carcinoma cell line designated CAOV3 were obtained from American Type Culture Collection (Rockville, MD).

Techniques: Over Expression, Control, Inhibition

(A) Compared to the IOSE cells, the expression of miR-373 was significantly down-regulated in all four EOC cell lines. The expression of miR-373 was the lowest in SKOV3 cells. EOC, epithelial ovarian cancer; IOSE, immortalized nontumorigenic human ovarian surface epithelial; * p < 0.05 and ** p < 0.01. (B) SKOV3 cells express high level of miR-373 after transfection with pMSCV-miR-373 compared to the mock control, *** p < 0.001. (C) The effect of miR-373 on morphological changes of SKOV3 cells. More rounded epithelial-like morphology was observed in the miR-373-transfected-SKOV3 cells (bottom), while spindle-shaped mesenchymal-like morphology was observed in the mock control cells (top). (D) E-cadherin (epithelial marker) augmentation and N-cadherin (mesenchymal marker) reduction in SKOV3 after the expression of miR-373. (E-F) Transwell invasion and migration assays of SKOV3 cells expressing miR-373 or mock control. Representative images (×100) are shown on the left and the quantification of five randomly selected fields is shown on the right. The invasive and migratory potential of miR-373 - expressing cells showed a strong reduction compared with mock controls. (G) Decreased cellular migration in miR-373-transfected SKOV3 cells was confirmed by wound scratch assay. (H-I) Representative bioluminescent images of disseminated tumor in nude mice i.p. injected with SKOV3 luc -pMSCV-miR-373 cells (bottom) and SKOV3 luc -pMSCV-NC cells (top), respectively. (J) The anatomical location of metastatic tumors upon macroscopic examination reflected bioluminescence and the number of metastatic tumor between two groups was significantly different, ** p < 0.01.

Journal: Oncotarget

Article Title: MiR-373 targeting of the Rab22a oncogene suppresses tumor invasion and metastasis in ovarian cancer

doi:

Figure Lengend Snippet: (A) Compared to the IOSE cells, the expression of miR-373 was significantly down-regulated in all four EOC cell lines. The expression of miR-373 was the lowest in SKOV3 cells. EOC, epithelial ovarian cancer; IOSE, immortalized nontumorigenic human ovarian surface epithelial; * p < 0.05 and ** p < 0.01. (B) SKOV3 cells express high level of miR-373 after transfection with pMSCV-miR-373 compared to the mock control, *** p < 0.001. (C) The effect of miR-373 on morphological changes of SKOV3 cells. More rounded epithelial-like morphology was observed in the miR-373-transfected-SKOV3 cells (bottom), while spindle-shaped mesenchymal-like morphology was observed in the mock control cells (top). (D) E-cadherin (epithelial marker) augmentation and N-cadherin (mesenchymal marker) reduction in SKOV3 after the expression of miR-373. (E-F) Transwell invasion and migration assays of SKOV3 cells expressing miR-373 or mock control. Representative images (×100) are shown on the left and the quantification of five randomly selected fields is shown on the right. The invasive and migratory potential of miR-373 - expressing cells showed a strong reduction compared with mock controls. (G) Decreased cellular migration in miR-373-transfected SKOV3 cells was confirmed by wound scratch assay. (H-I) Representative bioluminescent images of disseminated tumor in nude mice i.p. injected with SKOV3 luc -pMSCV-miR-373 cells (bottom) and SKOV3 luc -pMSCV-NC cells (top), respectively. (J) The anatomical location of metastatic tumors upon macroscopic examination reflected bioluminescence and the number of metastatic tumor between two groups was significantly different, ** p < 0.01.

Article Snippet: The human epithelial ovarian cancer (EOC) cells (SKOV3, A2780, and CP70) were purchased from the American Type Culture Collection (ATCC, Manassas, VA) and were cultured in RPMI-1640 (Gibco, Foster City, CA) supplemented with 10% (w/v) fetal bovine serum (FBS; Gibco) and 1% penicillin-streptomycin (Gibco).

Techniques: Expressing, Transfection, Control, Marker, Migration, Wound Healing Assay, Injection