The Tumor-Suppressive Effect of MicroRNA-375 on the Differentiated Gastric Adenocarcinoma, but Not on the Undifferentiated

Human cervical cancer is the most common gynecological malignancy. The continuous development of nanotechnology has allowed the wide use of nanomaterials in cancer treatment. Nanoparticles can be used as gene carriers because of their surface effect and small-size effect. MicroRNA-let-7c-5p (miR-let-7c-5p) belongs to the let-7 family. Although it has been reported to exert a tumor suppressive effect in a variety of cancers, the exact role and mechanism of miR-let-7c-5p in the progression of cervical cancer are unclear. In this study, we synthesized flower-shaped SiO2 –PEI nanoparticles with high pDNA/siRNA loading rates. This nanoparticle with miR-let-7c-5p-expressed plasmid could effectively transfer miR-let-7c-5p to human epithelial carcinoma (HeLa) cells. In addition, the combination of nanomaterials and gene therapy could inhibit the development of cancer under the conditions of extremely low cytotoxicity. These findings provided a new anticancer strategy based on F-SiO2 -polyethyleneimine/miR-let-7c-5p (FSP-let-7c-5p)nanoparticles and indicated that miR-let-7c-5p/IGF-1R/PI3K/AKT and -catenin/SLUG could be used as new potential targets for the treatment of cervical cancer.

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LncRNA MONC Suppresses the Malignant Phenotype of Endometrial Cancer Stem Cells by Regulating the MiR-636/GLCE Axis

10.21203/rs.3.rs-40559/v1 ◽

2020 ◽

Author(s):

Yibing Li ◽

Jianing Huo ◽

Junjian He ◽

Haining Ma ◽

Xiaoxin Ma

Keyword(s):

Cell Cycle ◽

Stem Cells ◽

Endometrial Cancer ◽

Cancer Stem Cells ◽

Suppressive Effect ◽

Luciferase Assay ◽

Biological Behavior ◽

Mesenchymal Transition ◽

Tumor Suppressive Effect

Abstract Background: Emerging evidence shows that abnormal expression of long non-coding RNA is involved in the occurrence and development of various tumors. LncRNA MONC is abnormally expressed in head and neck squamous cell carcinoma (HNSCC), lung cancer, colorectal cancer, and acute megakaryocytic leukemia, but the biological function and potential regulatory mechanism of MONC in endometrial cancer stem cells (ECSCs) and endometrial cancer cells (ECCs) have not been studied. In this study, we aimed to explore the tumor suppressive effect and mechanism of MONC in regulating ECSCs and ECCs. Methods: The expression of genes was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The expression of proteins was detected by Western blot. The interplay of LncRNA-miRNA-mRNA was verified using the luciferase assay. The growth rate of ECSC spheroids was detected by sphere formation assay. Cell proliferation was detected by CCK-8 assay. The cell invasion was detected by transwell invasion assay. Cell cycle was detected by Cell cycle analysis.Cell apoptosis was detected by the Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double-staining assay. Animal study was conducted to evaluate the effect of MONC combined with miR-636 on tumor growth in vivo. Results: Low MONC expression in endometrial carcinoma (EC), which directly inhibits the malignant biological behavior of ECSCs and ECCs by directly inhibiting miR-636. Simultaneously, miR-636 may indirectly reduce the expression of MONC. Down-regulation of miR-636 may promote GLCE expression by targeting the 3'-untranslated region (UTR) of the downstream gene GLCE, thereby inhibiting the progression of ECSCs. MONC combined with miR-636 inhibited the Notch signaling pathway and tumor epithelial-to-mesenchymal transition (EMT) process. In addition, we verified the tumor suppressive effect of MONC in nude mice, miR-636 can rescue the tumor suppressive effect of overexpressing MONC, and this effect is more obvious in ECSC. Conclusion: MONC inhibits the malignant phenotypes of ECSCs and ECCs by regulating the miR-636/GLCE axis. The MONC/miR-636/GLCE axis may provide novel treatment avenues for human EC.

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MicroRNA-27a-5p inhibits proliferation, migration and invasion and promotes apoptosis of Wilms tumor cell by targeting PBOV1

10.1101/2021.08.25.457737 ◽

2021 ◽

Author(s):

zhengtuan guo ◽

qiang yv ◽

chunlin miao ◽

wenan ge ◽

peng li

Keyword(s):

Tumor Cells ◽

Wilms Tumor ◽

Suppressive Effect ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Tumor Tissues ◽

And Function ◽

Tumor Suppressive Effect

Wilms tumor is the most common type of renal tumor in children. MicroRNAs (miRNA) are small non-coding RNAs that play crucial regulatory roles in tumorigenesis. We aimed to study the expression profile and function of miR-27a-5p in Wilms tumor. MiR-27a-5p expression was downregulated in human Wilms tumor tissues. Functionally, overexpression of miR-27a-5p promoted cell apoptosis of Wilms tumor cells. Furthermore, upregulated miR-27a-5p delayed xenograft Wilms tumor tumorigenesis in vivo. Bioinformatics analysis predicted miR-27-5p directly targeted to the 3’-untranslated region (UTR) of PBOV1 and luciferase reporter assay confirmed the interaction between miR-27a-5p and PBOV1. The function of PBOV1 in Wilms tumor was evaluated in vitro and knockdown of PBOV1 dampened cell migration. In addition, overexpression of PBOV1 antagonized the tumor-suppressive effect of miR-27a-5p in Wilms tumor cells. Collectively, our findings reveal the regulatory axis of miR-27-5p/PBOV1 in Wilms tumor and miR-27a-5p might serve as a novel therapeutic target in Wilms tumor.

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Propofol exhibits a tumor‑suppressive effect and regulates cell viability, migration and invasion in bladder carcinoma by targeting the microRNA‑10b/HOXD10 signaling pathway

Oncology Letters ◽

10.3892/ol.2019.10968 ◽

2019 ◽

Cited By ~ 1

Author(s):

Zongcai Qi ◽

Lei Yuan ◽

Nenghong Sun

Keyword(s):

Cell Viability ◽

Signaling Pathway ◽

Bladder Carcinoma ◽

Suppressive Effect ◽

Migration And Invasion ◽

Tumor Suppressive Effect

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Cyanidin-3-O-glucoside Inhibits the β-catenin/MGMT Pathway by Upregulating miR-214-5p to Reverse Chemotherapy Resistance in Glioma Cells

10.21203/rs.3.rs-783551/v1 ◽

2021 ◽

Author(s):

Yuan Zhou ◽

Li Chen ◽

Deping Ding ◽

Ziheng Li ◽

Li Cheng ◽

...

Keyword(s):

Cytotoxic Effect ◽

Opposite Effect ◽

Alkylating Agents ◽

Chemotherapy Resistance ◽

Glioma Cells ◽

Suppressive Effect ◽

Signaling Mechanism ◽

Induced Apoptosis ◽

Tumor Suppressive Effect

Abstract Overcoming resistance to alkylating agents has important clinical significance in glioma. Cyanidin-3-O-glucoside (C3G) has a tumor-suppressive effect on tumor cells. However, whether it plays a role in temozolomide resistance in glioma is still unclear. We construct a TMZ-resistant glioma LN-18/TR cells, observe the effect of C3G on TMZ resistance in these cells, and explore the role of miR-214-5p in chemoresistance.Results show that β-catenin and MGMT were significantly upregulated in LN-18/TR cells. C3G upregulated miR-214-5p and enhanced the cytotoxic effect of temozolomide on LN-18/TR cells. C3G downregulated β-catenin and MGMT. The miR-214-5p mimic downregulated β-catenin and MGMT in LN-18/TR cells, whereas the miR-214-5p inhibitor had the opposite effect. The miR-214-5p inhibitor significantly blocked the cyanidin-3-O-glucoside-induced downregulation of β-catenin and MGMT. C3G or the miR-214-5p mimic enhanced temozolomide-induced apoptosis in LN-18/TR cells, whereas the miR-214-5p inhibitor blocked this effect. Further, C3G or miR-214-5p agomir combined with TMZ could significantly inhibit the growth of LN-18/TR tumors. Our research has discovered the potential signaling mechanism associated with C3G-mediated suppression of TMZ resistance in LN-18/TR cells through miR-214-5p, which can facilitate the treatment of MGMT-induced resistance in glioma cells.

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Dual Role of α6β4 Integrin in Epidermal Tumor Growth: Tumor-suppressive Versus Tumor-promoting Function

Molecular Biology of the Cell ◽

10.1091/mbc.e06-08-0720 ◽

2007 ◽

Vol 18 (11) ◽

pp. 4210-4221 ◽

Cited By ~ 35

Author(s):

Karine Raymond ◽

Maaike Kreft ◽

Ji-Ying Song ◽

Hans Janssen ◽

Arnoud Sonnenberg

Keyword(s):

Tumor Growth ◽

Tumor Development ◽

Mouse Skin ◽

Suppressive Effect ◽

Mouse Tumor ◽

Tumor Initiating Cells ◽

Isolated Cells ◽

Laminin 5 ◽

Tumor Suppressive Effect

An increased expression of the integrin α6β4 is correlated with a poor prognosis in patients with squamous cell carcinomas. However, little is known about the role of α6β4 in the early stages of tumor development. We have isolated cells from mouse skin (mouse tumor-initiating cells [mTICs]) that are deficient in both p53 and Smad4 and carry conditional alleles of the β4 gene (Itgb4). The mTICs display many features of multipotent epidermal stem cells and produce well-differentiated tumors after subcutaneous injection into nude mice. Deletion of Itgb4 led to enhanced tumor growth, indicating that α6β4 mediates a tumor-suppressive effect. Reconstitution experiments with β4-chimeras showed that this effect is not dependent on ligation of α6β4 to laminin-5, but on the recruitment by this integrin of the cytoskeletal linker protein plectin to the plasma membrane. Depletion of plectin, like that of β4, led to increased tumor growth. In contrast, when mTICs had been further transformed with oncogenic Ras, α6β4 stimulated tumor growth, as previously observed in human squamous neoplasms. Expression of different effector-loop mutants of RasV12 suggests that this effect depends on a strong activation of the Erk pathway. Together, these data show that depending on the mutations involved, α6β4 can either mediate an adhesion-independent tumor-suppressive effect or act as a tumor promotor.

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