scholarly journals Characterization of a Novel Murine Colon Carcinoma Subline with High-Metastatic Activity Established by In Vivo Selection Method

2020 ◽  
Vol 21 (8) ◽  
pp. 2829
Author(s):  
Liqiu Ma ◽  
Yoshimitsu Sakamoto ◽  
Akinori Kanai ◽  
Hiromi Otsuka ◽  
Akihisa Takahashi ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Expression Profiles ◽  
Marked Change ◽  
Morphological Characteristics ◽  
Parental Cell ◽  
Parental Cell Line ◽  
Colon 26 ◽  
In Vivo Selection ◽  
Metastatic Activity

The establishment of cancer cell lines, which have different metastatic abilities compared with the parental cell, is considered as an effective approach to investigate mechanisms of metastasis. A highly metastatic potential mouse colon cancer cell subline, Colon-26MGS, was derived from the parental cell line Colon-26 by in vivo selection using continuous subcutaneous implanting to immunocompetent mice. To clarify the mechanisms involved in the enhancement of metastasis, morphological characteristics, cell proliferation, and gene expression profiles were compared between Colon-26MGS and the parental cell. Colon-26MGS showed over 10 times higher metastatic ability compared with the parental cell, but there were no differences in morphological characteristics and in vitro proliferation rates. In addition, the Colon-26MGS-bearing mice exhibited no marked change of splenocyte population and lung pre-metastatic niche with tumor-free mice, but there were significant differences compared to Colon-26-bearing mice. RNA-seq analyses indicated that immune costimulatory molecules were significantly up-regulated in Colon-26MGS. These results suggest that Colon-26MGS showed not only higher metastatic activity, but also less induction property of host immune response compared to parental Colon-26. Colon-26MGS has proven to be a novel useful tool for studying multiple mechanisms involving metastasis enhancement.

Regulation of c-met expression in B16 murine melanoma cells by melanocyte stimulating hormone

1999 ◽  
Vol 112 (5) ◽  
pp. 623-630
Author(s):  
D. Rusciano ◽  
P. Lorenzoni ◽  
M.M. Burger
Keyword(s):  
Melanoma Cells ◽  
Parental Cell ◽  
Melanocortin Receptor ◽  
Parental Cell Line ◽  
Melanocyte Stimulating Hormone ◽  
Murine Melanoma ◽  
The One ◽  
Murine Melanoma Cells ◽  
Stimulating Hormone

B16 murine melanoma cells selected in vivo for enhanced liver metastatic ability (B16-LS9) show on the one hand an increased expression and constitutive activation of the proto-oncogene c-met (the receptor for hepatocyte growth factor/scatter factor), and on the other hand a more differentiated phenotype, when compared to the parental cell line, B16-F1. Following this observation, we have tried to establish whether there is a direct relationship between differentiation and c-met expression in B16 melanoma cells. Treatment of these cells with differentiating agents indicated that c-met expression was strongly induced by melanocyte stimulating hormone, while retinoic acid had almost no influence. c-met induction was triggered by engagement of the melanocortin receptor, cAMP elevation and PKA/PKC(α) activation, as respectively shown by the effects of ACTH, cAMP elevating agents and specific PK inhibitors. Regulation of c-met expression via the melanocortin receptor and cAMP raises the intriguing possibility that autocrine and/or paracrine mechanisms acting in vivo on this circuit might influence (through c-met expression and activation) the metastatic behavior of these tumor cells, which we have shown to be dependent on their c-met expression.

scholarly journals cis Expression of DC-SIGN Allows for More Efficient Entry of Human and Simian Immunodeficiency Viruses via CD4 and a Coreceptor

2001 ◽  
Vol 75 (24) ◽  
pp. 12028-12038 ◽  
Author(s):  
Benhur Lee ◽  
George Leslie ◽  
Elizabeth Soilleux ◽  
Una O'Doherty ◽  
Sarah Baik ◽  
...  
Keyword(s):  
Cell Lines ◽  
Viral Entry ◽  
Parental Cell ◽  
Jurkat Cells ◽  
Target Cells ◽  
Parental Cell Line ◽  
Dependent Manner ◽  
Immunodeficiency Virus ◽  
T Cell Lines

ABSTRACT DC-SIGN is a C-type lectin expressed on dendritic cells and restricted macrophage populations in vivo that binds gp120 and acts intrans to enable efficient infection of T cells by human immunodeficiency virus type 1 (HIV-1). We report here that DC-SIGN, when expressed in cis with CD4 and coreceptors, allowed more efficient infection by both HIV and simian immunodeficiency virus (SIV) strains, although the extent varied from 2- to 40-fold, depending on the virus strain. Expression of DC-SIGN on target cells did not alleviate the requirement for CD4 or coreceptor for viral entry. Stable expression of DC-SIGN on multiple lymphoid lines enabled more efficient entry and replication of R5X4 and X4 viruses. Thus, 10- and 100-fold less 89.6 (R5/X4) and NL4–3 (X4), respectively, were required to achieve productive replication in DC-SIGN-transduced Jurkat cells when compared to the parental cell line. In addition, DC-SIGN expression on T-cell lines that express very low levels of CCR5 enabled entry and replication of R5 viruses in a CCR5-dependent manner, a property not exhibited by the parental cell lines. Therefore, DC-SIGN expression can boost virus infection in cis and can expand viral tropism without affecting coreceptor preference. In addition, coexpression of DC-SIGN enabled some viruses to use alternate coreceptors like STRL33 to infect cells, whereas in its absence, infection was not observed. Immunohistochemical and confocal microscopy data indicated that DC-SIGN was coexpressed and colocalized with CD4 and CCR5 on alveolar macrophages, underscoring the physiological significance of these cis enhancement effects.

In Vivo Selection of High-Metastatic Subline of Bladder Cancer Cell and its Characterization

2013 ◽  
Vol 20 (7) ◽  
pp. 289-295 ◽  
Author(s):  
Naoki Sugiyama ◽  
Mihoko Sutoh Yoneyama ◽  
Shingo Hatakeyama ◽  
Hayato Yamamoto ◽  
Akiko Okamoto ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cell ◽  
Bladder Cancer Cell ◽  
In Vivo Selection ◽  
Selection Of

scholarly journals Role and mechanism of miR-130a-3p in the chemosensitivity of retinoblastoma cells to vincristine

2021 ◽  
Author(s):  
Xiulan Lu ◽  
Huifang Tu ◽  
Dongrun Tang ◽  
Xiaoming Huang ◽  
Fengyuan Sun
Keyword(s):  
Drug Resistance ◽  
Cell Line ◽  
Resistance Index ◽  
Parental Cell ◽  
Luciferase Assay ◽  
Parental Cell Line ◽  
Pax6 Expression ◽  
Retinoblastoma Cells ◽  
Primary Obstacle

Abstract Purpose Chemoresistance remains the primary obstacle threatening the prognosis of retinoblastoma (RB). microRNAs (miRNAs) are acknowledged as critical regulator of drug resistance. This study explored the molecular mechanism of miR-130a-3p affecting the chemosensitivity of RB to vincristine (VCR). Methods miR-130a-3p expression of VCR-sensitive and VCR-resistant RB tissues was detected using RT-qPCR. VCR-resistant RB cell line Y79/VCR was induced. miR-130a-3p expression of Y79/VCR cell line and its corresponding parental cell line was detected. Y79/VCR cells were subjected to miR-130a-3p overexpression treatment. The cell proliferation was measured using MTT assay, and the IC50 value and drug resistance index were examined using CCK-8 assay. The targeting relationship between miR-130a-3p and PAX6 was predicted through bioinformatics analysis and verified using dual-luciferase assay. Functional rescue experiments were conducted to confirm the role of PAX6 in chemosensitivity of RB cells. The effect of miR-130a-3p on tumorigenesis and VCR sensitivity was observed in vivo. Results miR-130a-3p was downregulated in VCR-resistant RB tissues and cells. Overexpression of miR-130a-3p repressed the proliferation of VCR-resistant RB cells and enhanced chemosensitivity. miR-130a-3p targeted PAX6 expression. Overexpression of PAX6 reversed the effect of miR-130a-3p on chemosensitivity of RB. Overexpression of miR-130a-3p suppressed tumor growth and reduced VCR resistance in vivo. Conclusion miR-130a-3p enhanced the chemosensitivity of RB cells to VCR by targeting PAX6 expression.

CT-707 Overcomes Resistance of Crizotinib through Activating PDPK1- AKT1 Pathway by Targeting FAK

2019 ◽  
Vol 19 (8) ◽  
pp. 655-665
Author(s):  
Caixia Liang ◽  
Ningning Zhang ◽  
Qiaoyun Tan ◽  
Shuxia Liu ◽  
Rongrong Luo ◽  
...  
Keyword(s):  
Kinase Inhibitors ◽  
Xenograft Model ◽  
Therapy Resistance ◽  
Parental Cell ◽  
Parental Cell Line ◽  
Antitumor Effects ◽  
Anaplastic Lymphoma ◽  
Promising Therapeutic Agent

Background: Crizotinib established the position of anaplastic lymphoma kinase-tyrosine kinase inhibitors (ALK-TKI) in the treatment of non-small cell lung cancer (NSCLC) while the therapy- resistance hindered those patients from benefitting continuously from the treatment. CT-707 is an inhibitor of ALK/focal adhesion kinase (FAK) and IGFR-1. H2228CR (crizotinib resistance, CR) and H3122CR NSCLC cell lines were generated from the parental cell line H2228 (EML4-ALK, E6a/b:A20, variant 3) and H3122(EML4-ALK, E13:A20, variant 1), respectively. Methods: We investigated the antitumor effects CT-707 exerted against H3122CR in vitro /vivo. Results: Importantly, our study provided evidence that CT-707 overcomes resistance to crizotinib through activating PDPK1-AKT1 pathway by targeting FAK. Meanwhile, by using an in-vivo H3122CR xenograft model, we found CT-707 inhibited tumor growth significantly without obvious side effects. Conclusion: These findings indicate that CT-707 may be a promising therapeutic agent against crizotinib- resistance in NSCLC.

scholarly journals Inhibition of glutaminase expression by antisense mRNA decreases growth and tumourigenicity of tumour cells

2000 ◽  
Vol 348 (2) ◽  
pp. 257-261 ◽  
Author(s):  
Carolina LOBO ◽  
Miguel A. RUIZ-BELLIDO ◽  
Juan C. ALEDO ◽  
Javier MÁRQUEZ ◽  
Ignacio NÚÑEZ DE CASTRO ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Critical Role ◽  
Parental Cell ◽  
Terminal Segment ◽  
Transformation Process ◽  
Tumour Cells ◽  
Parental Cell Line ◽  
Transfected Cells ◽  
Antisense Mrna

Phosphate-activated glutaminase has a critical role in tumours and rapidly dividing cells and its activity is correlated with malignancy. Ehrlich ascites tumour cells transfected with the pcDNA3 vector containing an antisense segment (0.28 kb) of rat kidney glutaminase showed impairment in the growth rate and plating efficiency, as well as a shortage in the glutaminase protein and activity. The C-terminal segment used is well conserved in all glutaminase sequences known. The transfected cells, named 0.28AS-2, displayed remarkable changes in their morphology compared with the parental cell line. The 0.28AS-2 cells also lost their tumourigenic capacity in vivo. Control mice developed an ascitic tumour, with a lifespan of 16±1 days, when inoculated with 107 cells/mouse; on the contrary, animals inoculated with transfected cells up to 2.5 times the cell numbers of control mice did not develop tumours and behaved as healthy animals. The ability to revert the transformed phenotype of antisense-transfected cells confirms the relevance of glutaminase in the transformation process and could provide new ways for the study of gene therapy.

scholarly journals Linc00518 Contributes to Multidrug Resistance Through Regulating the MiR-199a/MRP1 Axis in Breast Cancer

2018 ◽  
Vol 48 (1) ◽  
pp. 16-28 ◽  
Author(s):  
Liang Chang ◽  
Zhuang Hu ◽  
Zhenyu Zhou ◽  
Hui Zhang
Keyword(s):  
Breast Cancer ◽  
Multidrug Resistance ◽  
Molecular Mechanisms ◽  
Drug Susceptibility ◽  
Parental Cell ◽  
Luciferase Reporter ◽  
Parental Cell Line ◽  
Normal Tissues ◽  
Mcf 7

Background/Aims: Long non-coding RNAs (LncRNAs) have been validated to be pivotal mediators in multidrug resistance (MDR) of various cancers. This study aims to explore the roles and molecular mechanisms of linc00518 implicated in chemoresistance in breast cancer. Methods: Expressions of linc00518, miR-199a and MRP1 were evaluated by RT-qPCR or western blot. IC50 values of adriamycin (ADR), vincristine (VCR) and paclitaxel (PTX) were determined by XTT assays and cell apoptosis was assessed by flow cytometry. Luciferase reporter and RIP assays were employed to detect the interaction of linc00518, miR-199a and MRP-1. Results: linc00518 expression increased nearly 2 fold and MRP1 level elevated about 2.5 fold in breast cancer tissues as compared to that in adjacent normal tissues. Also, almost 2 fold upregulation of linc00518 and MRP-1 expressions was observed in MCF-7 cells than in MCF-10A cells. Additionally, linc00518 level was almost 2.5 fold higher and MRP1 level was about 2 fold increased in ADR-resistant MCF-7 cells (MCF-7/ADR) than in parental cell line MCF-7. Linc00518 knockdown enhanced chemosensitivity to ADR, VCR and PTX, and boosted ADR-, VCR- and PTX-induced apoptosis in MCF-7/ADR cells. miR-199a inhibitor conferred chemoresistance to ADR, VCR and PTX in MCF-7/ADR cells, and suppressing miR-199a reversed multi-drug susceptibility induced by linc00518 knockdown. Furthermore, linc00518 could act as a molecular sponge of miR-199a to repress MRP1 expression. MRP1 depletion increased the sensitivity of MCF-7/ADR cells to ADR, VCR and PTX, and this effect was attenuated following miR-199a inhibition or linc00518 overexpression. Also, linc00518 silencing increased ADR-mediated anti-tumor effect in vivo. Conclusions: linc00518 downregulation reduced MDR by regulating miR-199a/MRP1 axis in breast cancer.

scholarly journals Adriamycin-resistant cells are significantly less fit than adriamycin-sensitive cells in cervical cancer

2021 ◽  
Vol 16 (1) ◽  
pp. 53-60
Author(s):  
Min Qi ◽  
Lijuan Xie ◽  
Guihua Duan
Keyword(s):  
Parental Cell ◽  
Parental Cell Line ◽  
G1 Arrest ◽  
Lower Growth ◽  
Chemotherapy Agent ◽  
Cytotoxic Treatment ◽  
Cell Line Hela ◽  
Resistant Cells

Abstract Adriamycin (ADR) is an important chemotherapy agent in many advanced cancers, but the emergence of drug resistance during treatment is a major limitation to its successful use. Recent studies have suggested that drug-resistant cells become less fit and their growth could be inhibited by parental cells without cytotoxic treatment. In this study, we examined the fitness differences between HeLa and HeLa/ADR cells. Compared with the parental cell line, HeLa/ADR cells showed significantly lower growth rates, both in vitro and in vivo. There was no difference in the apoptosis rate between them, but G1 arrest and reduced DNA synthesis were found in HeLa/ADR cells. Further study indicated that HeLa/ADR cells failed to compete for space and nutrition against parental cells in vivo. Taken together, we demonstrate that HeLa/ADR cells are less fit and their growth can be inhibited by parental cells in the absence of ADR; therefore, the maintenance of a certain amount of ADR-sensitive cells during treatment may facilitate the control of the development of ADR resistance.

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