Direct In Vivo Xenograft Tumor Model for Predicting Chemotherapeutic Drug Response in Cancer Patients

2008 ◽  
Vol 85 (2) ◽  
pp. 217-221 ◽  
Author(s):  
B Rubio-Viqueira ◽  
M Hidalgo
Keyword(s):  
Cancer Patients ◽  
Drug Response ◽  
Tumor Model ◽  
Chemotherapeutic Drug ◽  
Xenograft Tumor ◽  
Xenograft Tumor Model

scholarly journals Circular RNA circ-CDYL sponges miR-1180 to elevate yes-associated protein in multiple myeloma

2020 ◽  
Vol 245 (11) ◽  
pp. 925-932 ◽  
Author(s):  
Fang Chen ◽  
Xiaohui Wang ◽  
Shuang Fu ◽  
Shaokun Wang ◽  
Yu Fu ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Tumor Model ◽  
Circular Rna ◽  
Xenograft Tumor ◽  
Functional Assays ◽  
Xenograft Tumor Model ◽  
Therapeutic Possibility ◽  
Plasma Depletion ◽  
Potential Therapeutic Intervention

The covalently closed circular RNA has recently been proposed as a pivotal player in tumorigenesis. In the current study, we found that circ-CDYL was notably elevated in multiple myeloma tissue and plasma samples and had good diagnostic and prognostic efficacy. Functional assays showed that circ-CDYL enhanced the viability and DNA synthesis of multiple myeloma cells and inhibited apoptosis. Mechanically, cytoplasmic circ-CDYL was co-localized with miR-1180, and circ-CDYL absorbed miR-1180 to upregulate yes-associated protein (YAP), thereby facilitating multiple myeloma progression. Importantly, we further confirmed the existence of this circ-CDYL/miR-1180/YAP regulatory axis in vivo by using the xenograft tumor model. Taken together, our data demonstrate that circ-CDYL is novel promoter of multiple myeloma, and targeting circ-CDYL and its associated network implicates the therapeutic possibility for multiple myeloma patients. Impact statement Multiple myeloma (MM) is an extremely complex and heterogeneous disease, and its pathogenesis is poorly understood. Here, we described an important MM-related circular RNA (circRNA), circ-CDYL. It was remarkably increased in both MM cells and plasma. Depletion of circ-CDYL evidently stunted MM growth. Circ-CDYL could absorb miR-1180 and alleviated the repression of miR-1180 on YAP, leading to increased YAP expression, ultimately triggering MM uncontrolled growth. Therefore, our findings advance the understanding of MM pathogenesis, and also raise the possibility of considering circ-CDYL as a potential therapeutic intervention for MM.

scholarly journals mTORC2 promotes cell survival through c-Myc–dependent up-regulation of E2F1

2015 ◽  
Vol 211 (1) ◽  
pp. 105-122 ◽  
Author(s):  
Zhipeng Zou ◽  
Juan Chen ◽  
Anling Liu ◽  
Xuan Zhou ◽  
Qiancheng Song ◽  
...  
Keyword(s):  
Cell Survival ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
In Vivo Experiments ◽  
Xenograft Tumor Model ◽  
Cancer Cell Survival ◽  
Consequent Reduction ◽  
Dependent Mechanism

Previous studies have reported that mTORC2 promotes cell survival through phosphorylating AKT and enhancing its activity. We reveal another mechanism by which mTORC2 controls apoptosis. Inactivation of mTORC2 promotes binding of CIP2A to PP2A, leading to reduced PP2A activity toward c-Myc serine 62 and, consequently, enhancement of c-Myc phosphorylation and expression. Increased c-Myc activity induces transcription of pri-miR-9-2/miR-9-3p, in turn inhibiting expression of E2F1, a transcriptional factor critical for cancer cell survival and tumor progression, resulting in enhanced apoptosis. In vivo experiments using B cell–specific mTORC2 (rapamycin-insensitive companion of mTOR) deletion mice and a xenograft tumor model confirmed that inactivation of mTORC2 causes up-regulation of c-Myc and miR-9-3p, down-regulation of E2F1, and consequent reduction in cell survival. Conversely, Antagomir-9-3p reversed mTORC1/2 inhibitor–potentiated E2F1 suppression and resultant apoptosis in xenograft tumors. Our in vitro and in vivo findings collectively demonstrate that mTORC2 promotes cell survival by stimulating E2F1 expression through a c-Myc– and miR-9-3p–dependent mechanism.

Nano-Encapsulation of Plitidepsin: In Vivo Pharmacokinetics, Biodistribution, and Efficacy in a Renal Xenograft Tumor Model

2013 ◽  
Vol 31 (4) ◽  
pp. 983-991 ◽  
Author(s):  
Hugo Oliveira ◽  
Julie Thevenot ◽  
Elisabeth Garanger ◽  
Emmanuel Ibarboure ◽  
Pilar Calvo ◽  
...  
Keyword(s):  
Tumor Model ◽  
Xenograft Tumor ◽  
Xenograft Tumor Model ◽  
In Vivo Pharmacokinetics

scholarly journals A Novel Anti-EGFR mAb Ame55 with Lower Toxicity and Better Efficacy than Cetuximab When Combined with Irinotecan

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Weiyi Qiu ◽  
Chang Zhang ◽  
Shuang Wang ◽  
Xiaoyan Yu ◽  
Qiong Wang ◽  
...  
Keyword(s):  
Tumor Model ◽  
Phage Library ◽  
Lovo Cell ◽  
Xenograft Tumor ◽  
Cynomolgus Monkeys ◽  
Lower Affinity ◽  
Egfr Inhibition ◽  
Xenograft Tumor Model

To improve efficacy and minimize toxicity of EGFR inhibition treatment, we developed Ame55, a novel anti-EGFR IgG1 with lower affinity to EGFR than cetuximab (C225) from a human phage library. Ame55 had lower bioactivity than cetuximab in vitro but similar antitumor efficacy as cetuximab in vivo. Moreover, Ame55 was more efficacious than cetuximab in a Lovo cell xenograft tumor model when combined with irinotecan (CPT-11). Ame55 concentrates in the mouse xenograft tumor and has less toxicity than cetuximab in cynomolgus monkeys in an overdose study.

scholarly journals LncRNA SNHG15 regulates osteosarcoma progression in vitro and in vivo via sponging miR-346 and regulating TRAF4 expression

2020 ◽  
Vol 15 (1) ◽  
pp. 423-436
Author(s):  
Xuewu Chen ◽  
Hongguang Xu
Keyword(s):  
Binding Sites ◽  
Biological Function ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Positive Effects ◽  
Xenograft Tumor Model ◽  
Nucleolar Rna ◽  
Common Primary Malignant Bone

AbstractOsteosarcoma (OS) is a common primary malignant bone tumor around the world. It has been reported that long noncoding RNAs (lncRNAs) take part in diverse pathological processes of OS; however, the mechanism remains unknown. This study aimed to uncover the profile of lncRNA small nucleolar RNA host gene 15 (SNHG15), its biological function, and its potential involvement in the mechanism of OS progression in vitro and in vivo. The expression of SNHG15 and TRAF4 was promoted in OS tissues opposite for that of miR-346. The silencing of SNHG15 limited the proliferation, invasion, and enhanced apoptosis of SaoS2 and HOS cells. Moreover, the putative binding sites between miR-346 and SNHG15 or TRAF4 were predicted by starBase and Targetscan software online, individually. Also, miR-346 deletion reversed the positive effects of SNHG15 elimination on proliferation, apoptosis, and invasion in cells. In addition, the upregulation of TRAF4 disrupted the biofunctional results from miR-346 promotion subsequently. Finally, SNHG15 knockdown repressed OS tumor growth in a xenograft tumor model. SNHG15 enhanced the progression of OS by regulating the miR-346/TRAF4 axis in vitro and in vivo.

scholarly journals Combining Sodium Butyrate With Cisplatin Increases the Apoptosis of Gastric Cancer In Vivo and In Vitro via the Mitochondrial Apoptosis Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Yangbo Li ◽  
Pengzhan He ◽  
Yinghui Liu ◽  
Mingming Qi ◽  
Weiguo Dong
Keyword(s):  
Sodium Butyrate ◽  
Intestinal Flora ◽  
Tumor Model ◽  
Mitochondrial Apoptosis ◽  
Xenograft Tumor ◽  
Mouse Xenograft ◽  
Xenograft Tumor Model ◽  
Related Pathway

Introduction: The gastrointestinal malignancy, gastric cancer (GC), has a high incidence worldwide. Cisplatin is a traditional chemotherapeutic drug that is generally applied to treat cancer; however, drug tolerance affects its efficacy. Sodium butyrate is an intestinal flora derivative that has general anti-cancer effects in vitro and in vivo via pro-apoptosis effects and can improve prognosis in combination with traditional chemotherapy drugs. The present study aimed to assess the effect of sodium butyrate combined with cisplatin on GC.Methods: A Cell Counting Kit-8 assay was used to assess the viability of GC cells in vitro. Hoechst 33,258 staining and Annexin V-Phycoerythrin/7-Aminoactinomycin D were used to qualitatively and quantitatively detect apoptosis in GC cells. Intracellular reactive oxygen species (ROS) measurement and a mitochondrial membrane potential (MMP) assay kit were used to qualitatively and quantitatively reflect the function of mitochondria in GC cells. Western blotting was used to verify the above experimental results. A nude mouse xenograft tumor model was used to evaluate the anti-tumor efficacity of sodium and cisplatin butyrate in vivo.Results: Cisplatin combined with sodium butyrate increased the apoptosis of GC cells. In the nude mouse xenograft tumor model, sodium butyrate in combination with cisplatin markedly inhibited the growth of the tumor more effectively than either single agent. The combination of sodium butyrate and cisplatin increased the intracellular ROS, decreased the MMP, and suppressed the invasion and migration abilities of GC cells. Western blotting verified that the combination of sodium butyrate and cisplatin remarkably enhanced the levels of mitochondrial apoptosis-related pathway proteins.Conclusion: Sodium butyrate, a histone acetylation inhibitor produced by intestinal flora fermentation, combined with cisplatin enhanced the apoptosis of GC cells through the mitochondrial apoptosis-related pathway, which might be considered as a therapeutic option for GC.

In vivo efficacy of the recombinant anti-CD64 immunotoxin H22(scFv)-ETA′ in a human acute myeloid leukemia xenograft tumor model

2011 ◽  
Vol 129 (5) ◽  
pp. 1277-1282 ◽  
Author(s):  
Mehmet Kemal Tur ◽  
Michael Huhn ◽  
Edgar Jost ◽  
Theo Thepen ◽  
Tim H. Brümmendorf ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
In Vivo Efficacy ◽  
Xenograft Tumor Model ◽  
Human Acute Myeloid Leukemia ◽  
Acute Myeloid

scholarly journals m6A Modification-Mediated DUXAP8 Regulation of Malignant Phenotype and Chemotherapy Resistance of Hepatocellular Carcinoma Through miR-584-5p/MAPK1/ERK Pathway Axis

2021 ◽  
Vol 9 ◽  
Author(s):  
Zefeng Liu ◽  
Jin Lu ◽  
He Fang ◽  
Jiyao Sheng ◽  
Mengying Cui ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Poor Prognosis ◽  
Chemotherapy Resistance ◽  
Tumor Model ◽  
Mechanistic Study ◽  
Xenograft Tumor ◽  
Malignant Phenotype ◽  
Sorafenib Treatment ◽  
Xenograft Tumor Model

Hepatocellular carcinoma (HCC) has a poor prognosis due to its high malignancy, rapid disease progression, and the presence of chemotherapy resistance. Long-stranded non-coding RNAs (lncRNAs) affect many malignant tumors, including HCC. However, their mechanism of action in HCC remains unclear. This study aimed to clarify the role of DUXAP8 in regulating the malignant phenotype and chemotherapy resistance in HCC. Using an in vivo xenograft tumor model, the regulatory functions and mechanisms of lncRNA DUXAP8 in the progression and response of HCC to chemotherapy were explored. It was found that DUXAP8 was significantly upregulated in a patient-derived xenograft tumor model based on sorafenib treatment, which is usually associated with a relatively poor prognosis in patients. In HCC, DUXAP8 maintained its upregulation in the expression by increasing the stability of m6A methylation-mediated RNA. DUXAP8 levels were positively correlated with the proliferation, migration, invasion, and chemotherapy resistance of HCC in vivo and in vitro. In the mechanistic study, it was found that DUXAP8 competitively binds to miR-584-5p through a competing endogenous RNA (ceRNA) mechanism, thus acting as a molecular sponge for miR-584-5p to regulate MAPK1 expression, which in turn activates the MAPK/ERK pathway. These findings can provide ideas for finding new prognostic indicators and therapeutic targets for patients with HCC.

scholarly journals Niclosamide Exhibits Potent Anticancer Activity and Synergizes with Sorafenib in Human Renal Cell Cancer Cells

2018 ◽  
Vol 47 (3) ◽  
pp. 957-971 ◽  
Author(s):  
Xinyi Yu ◽  
Feng Liu ◽  
Liyi Zeng ◽  
Fang He ◽  
Ruyi Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Renal Cell ◽  
Cell Cancer ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Xenograft Tumor Model

Background/Aims: As the most lethal urological cancers, renal cell carcinoma (RCC) comprises a heterogeneous group of cancer with diverse genetic and molecular alterations. There is an unmet clinical need to develop efficacious therapeutics for advanced, metastatic and/or relapsed RCC. Here, we investigate whether anthelmintic drug Niclosamide exhibits anticancer activity and synergizes with targeted therapy Sorafenib in suppressing RCC cell proliferation. Methods: Cell proliferation and migration were assessed by Crystal violet staining, WST-1 assay, cell wounding and cell cycle analysis. Gene expression was assessed by qPCR. In vivo anticancer activity was assessed in xenograft tumor model. Results: We find that Niclosamide effectively inhibits cell proliferation, cell migration and cell cycle progression, and induces apoptosis in human renal cancer cells. Mechanistically, Niclosamide inhibits the expression of C-MYC and E2F1 while inducing the expression of PTEN in RCC cells. Niclosamide is further shown to synergize with Sorafenib in suppressing RCC cell proliferation and survival. In the xenograft tumor model, Niclosamide is shown to effectively inhibit tumor growth and suppress RCC cell proliferation. Conclusions: Niclosamide may be repurposed as a potent anticancer agent, which can potentiate the anticancer activity of the other agents targeting different signaling pathways in the treatment of human RCC.

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