Inhibition of glyoxalase-I leads to decreased proliferation and migration of high proliferative HCC tumor cell lines

Objective: Wilm’s tumor is a common renal malignancy in childhood with unsatisfactory prognosis. microRNA-215-5p (miR-215-5p) has been reported as a tumor-suppressive miRNA in different types of human cancers, but rarely in the Wilm’s tumor. In light of this, we tried to investigate the regulatory role and underlying mechanism of miR-215-5p in the Wilm’s tumor. Methods: After sample collection and cell culture, the expression of miR-215-5p and CT10 Regulator of Kinase (CRK) was detected. Then rhabdoid tumor cell lines (formerly classified as Wilms’ tumor cell lines), G401 and WT-CLS1 cells were transfected with pcDNA3.1, pcDNA3.1-CRK, sh-NC, sh-CRK, agomir NC, miR-215-5p agomir, antagomir NC or miR-215-5p antagomir to explore the function of miR-215-5p and CRK in the Wilm’s tumor cell proliferation and migration. Moreover, the relationship between miR-215-5p and CRK was analyzed by dual luciferase reporter gene assay. Results: Lowly-expressed miR-215-5p and highly-expressed CRK were observed in the Wilm’s tumor tissues and cells. Transfection of pcDNA3.1-CRK or miR-215-5p antagomir could promote G401 and WT-CLS1 cell proliferation and enhance migration ability, while transfection of sh-CRK or miR-215-5p agomir led to opposite results. Additionally, miR-215-5p may bind to CRK. Moreover, transfection of pcDNA3.1-CRK in G401 and WT-CLS1 cells could partially reverse the inhibitory effect of miR-215-5p agomir on the proliferation and migration of Wilm’s tumor cells. Conclusion: Our study highlighted that miR-215-5p could suppress the proliferation and migration of Wilm’s tumor cells by regulating the expression of CRK, providing new ideas for molecular targeted therapy for Wilm’s tumor.

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B7-H6, an immunoligand for the natural killer cell activating receptor NKp30, reveals inhibitory effects on cell proliferation and migration, but not apoptosis, in cervical cancer derived-cell lines

BMC Cancer ◽

10.1186/s12885-020-07608-4 ◽

2020 ◽

Vol 20 (1) ◽

Author(s):

Nehla Banu ◽

Annie Riera-Leal ◽

Jesse Haramati ◽

Pablo Cesar Ortiz-Lazareno ◽

Sandeep Surendra Panikar ◽

...

Keyword(s):

Cervical Cancer ◽

Flow Cytometry ◽

Cell Proliferation ◽

Tumor Cell ◽

Tumor Cells ◽

Cell Lines ◽

Cellular Localization ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

Abstract Background Although great progress has been made in treatment regimens, cervical cancer remains as one of the most common cancer in women worldwide. Studies focusing on molecules that regulate carcinogenesis may provide potential therapeutic strategies for cervical cancer. B7-H6, an activating immunoligand expressed by several tumor cells, is known to activate NK cell-mediated cytotoxicity once engaged with its natural receptor NKp30. However, the opposite, that is, the effects in the tumor cell triggered by B7-H6 after interacting with NKp30 has not yet been well explored. Methods In this study, we evaluated the surface expression of B7-H6 by flow cytometry. Later, we stimulated B7-H6 positive cervical cancer derived-cell lines (HeLa and SiHa) with recombinant soluble NKp30 (sNKp30) protein and evaluated biological effects using the impedance RTCA system for cell proliferation, the scratch method for cell migration, and flow cytometry for apoptosis. Cellular localization of B7-H6 was determined using confocal microscopy. Results Notably, we observed that the addition of sNKp30 to the cervical cancer cell lines decreased tumor cell proliferation and migration rate, but had no effect on apoptosis. We also found that B7-H6 is selectively maintained in tumor cell lines, and that efforts to sort and purify B7-H6 negative or positive cells were futile, as negative cells, when cultured, regained the expression of B7-H6 and B7-H6 positive cells, when sorted and cultivated, lost a percentage of B7-H6 expression. Conclusions Our results suggest that B7-H6 has an important, as of yet undescribed, role in the biology of the cervical tumor cells themselves, suggesting that this protein might be a promising target for anti-tumor therapy in the future.

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Serum and Glucocorticoid Inducible Kinase 1-Sensitive Survival, Proliferation and Migration of Rhabdomyosarcoma Cells

Cellular Physiology and Biochemistry ◽

10.1159/000481842 ◽

2017 ◽

Vol 43 (3) ◽

pp. 1301-1308 ◽

Cited By ~ 2

Author(s):

Evi Schmid ◽

Matias Julian Stagno ◽

Jing Yan ◽

Sabine Schleicher ◽

Willi Yu ◽

...

Keyword(s):

Cell Proliferation ◽

Tumor Cell ◽

Cell Survival ◽

Cell Lines ◽

Therapy Resistance ◽

Tumor Cell Survival ◽

Rhabdomyosarcoma Cell ◽

And Migration ◽

Tumor Types ◽

Proliferation And Migration

Background/Aims: Rhabdomyosarcoma, the most common pediatric soft tissue sarcoma, may show an intrinsic refractoriness to standard chemotherapy in advanced tumor stages, which is associated with poor prognosis. Cellular mechanisms conferring tumor cell survival and therapy resistance in many tumor types include the serum & glucocorticoid inducible kinase (SGK) 1 pathway, a kinase expressed ubiquitously with particularly strong expression in skeletal muscle and some tumor types. The present study explored whether SGK1 is expressed in rhabdomyosarcoma and, if so, whether this kinase impacts on tumor cell survival, proliferation and migration. Multiple in vitro techniques were used to study the role of SGK1 in rhabdomyosarcoma. Methods: The Gene Chip® Human Genome U133 Plus 2.0 Array were employed to examine SGK1 transcriptional activity in healthy muscle and rhabdomyosarcoma tissue. SGK1 transcript levels were quantified in rhabdomyosarcoma cell lines RD (embryonal subtype) and RH30 (alveolar subtype) by RT-PCR, cell viability was measured using MTT assays. Clonal cell growth was assessed via colony forming assays and migration experiments were performed in a transwell system. Results: SGK1 is expressed in embryonal and alveolar rhabdomyosarcoma tissue samples and in RD and RH30 rhabdomyosarcoma cell lines. Administration of EMD638683 – an inhibitor specific for SGK1 - decreased viability of RD and RH30 cells, enhanced the effects of the cytotoxic drug doxorubicin leading to reduced migration and decreased cell proliferation. Conclusions: SGK1 is expressed in rhabdomyosarcoma cells where it contributes to survival, therapy resistance, cell proliferation and migration. Thus, SGK1 inhibitors may be considered a therapeutic option for the treatment of therapy-resistant rhabdomyosarcoma.

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Role of I-TAC-binding receptors CXCR3 and CXCR7 in proliferation, activation of intracellular signaling pathways and migration of various tumor cell lines.

Folia Histochemica et Cytobiologica ◽

10.2478/v10042-008-0091-7 ◽

2010 ◽

Vol 48 (1) ◽

Cited By ~ 15

Author(s):

Katarzyna Miekus ◽

Danuta Jarocha ◽

Elzbieta Trzyna ◽

Marcin Majka

Keyword(s):

Tumor Cell ◽

Signaling Pathways ◽

Cell Lines ◽

Intracellular Signaling ◽

Tumor Cell Lines ◽

Intracellular Signaling Pathways ◽

And Migration

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Expression of HIF-1a and VEGF in human pituitary tumors and rodent pituitary tumor cell lines under hypoxia-mimicking condition

Experimental and Clinical Endocrinology & Diabetes ◽

10.1055/s-0028-1096352 ◽

2008 ◽

Vol 116 (09) ◽

Author(s):

B Shan ◽

C Onofri ◽

M Theodoropoulou ◽

E Arzt ◽

GK Stalla ◽

...

Keyword(s):

Tumor Cell ◽

Cell Lines ◽

Pituitary Tumor ◽

Pituitary Tumors ◽

Tumor Cell Lines ◽

Human Pituitary ◽

Pituitary Tumor Cell

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Interaction of Human Tumor Cells with Human Platelets and the Coagulation System

Thrombosis and Haemostasis ◽

10.1055/s-0038-1665296 ◽

1983 ◽

Vol 50 (03) ◽

pp. 726-730 ◽

Cited By ~ 11

Author(s):

Hamid Al-Mondhiry ◽

Virginia McGarvey ◽

Kim Leitzel

Keyword(s):

Tumor Cell ◽

Tumor Cells ◽

Cell Lines ◽

Human Tumor ◽

Human Platelets ◽

Factor Vii ◽

Coagulation System ◽

Breast Adenocarcinoma ◽

Activate Factor ◽

Tumor Cell Lines

SummaryThis paper reports studies on the interaction between human platelets, the plasma coagulation system, and two human tumor cell lines grown in tissue culture: Melanoma and breast adenocarcinoma. The interaction was monitored through the use of 125I- labelled fibrinogen, which measures both thrombin activity generated by cell-plasma interaction and fibrin/fibrinogen binding to platelets and tumor cells. Each tumor cell line activates both the platelets and the coagulation system simultaneously resulting in the generation of thrombin or thrombin-like activity. The melanoma cells activate the coagulation system through “the extrinsic pathway” with a tissue factor-like effect on factor VII, but the breast tumor seems to activate factor X directly. Both tumor cell lines activate platelets to “make available” a platelet- derived procoagulant material necessary for the conversion of prothrombin to thrombin. The tumor-derived procoagulant activity and the platelet aggregating potential of cells do not seem to be inter-related, and they are not specific to malignant cells.

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