Down-regulation of miR-203a by lncRNA PVT1 in multiple myeloma promotes cell proliferation

Yang, Man; Zhang, Lingxiu; Wang, Xiufeng; Zhou, Yanjun; Sun, Wei

doi:10.5114/aoms.2018.73975

Cited by 42 publications

(39 citation statements)

References 19 publications

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“…ose data indicated that suppression of KIF22 inhibited cell proliferation in vitro. Although the results are different, we also could use similar methods to explore the mechanism [39][40][41].…”

Section: Discussionmentioning

confidence: 99%

Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Tongue Squamous Cell Carcinoma

Liu

Ren

et al. 2020

BioMed Research International

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Background. Oral carcinoma is the sixth most common cancer and is a serious public health problem, and tongue squamous cell carcinoma (TSCC) is the most common type of oral carcinoma. Kinesin family member 22 (KIF22), also called as kinesin-like DNA binding protein (KID), is a microtubule-based motor protein and binds to both microtubules and chromosomes, transporting organelles, protein, and mRNA. This research aimed at investigating the prognostic significance of KIF22 in TSCC. Patients and Methods. This retrospective research collected 82 paired tissues with TSCC. KIF22 protein expression level was detected by immunohistochemical staining. Suppression of KIF22 with shRNA in CAL-27 and SCC-15 cells was to observe cell proliferation in vitro and xenograft tumor growth in vivo. Results. In TSCC tissues, the protein expression level of KIF22 was increased and correlated with tumor stage, clinical stage, and lymphatic metastasis (P=0.013, P=0.034 and P=0.015, respectively). Suppression of KIF22 inhibited cell proliferation and xenograft tumor growth. Conclusion. KIF22 might play an important role in the progression of TSCC and could serve as a therapeutic target for TSCC.

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Section: Discussionmentioning

confidence: 99%

Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Tongue Squamous Cell Carcinoma

Liu

Ren

et al. 2020

BioMed Research International

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“…Apart from MIAT, many lncRNAs were reported to play an active role in many pathogeneses of human diseases. For example, lncRNA PVT1 was once reported to represent a potential therapeutic target for the treatment of multiple myeloma because it could promote multiple myeloma cell proliferation and induce cell apoptosis by inhibiting its target gene, miR-203a [48]. And lncRNA, UBE2CP3-001, was found to be potentially applied in the anti-glioma therapy [49].…”

Section: Discussionmentioning

confidence: 99%

Rs1894720 polymorphism is associated with the risk of age-related cataract by regulating the proliferation of epithelial cells in the lens via the signalling pathway of MIAT/miR-26b/BCL2L2

Zhang

et al. 2020

Arch Med Sci

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Introduction: Cataracts caused by old age are one of the most frequent causes for blindness and poor vision worldwide. In this study, we aimed to clarify the possible role of rs1894720 polymorphism in the pathogenesis of age-related cataract. Material and methods: Rs1894720 polymorphism genotype was detected by TaqMan. Bioinformatics analysis, luciferase assay, real-time PCR, western blot, and protein density analysis were conducted to establish the correlations between MIAT and miR-26b as well as between BCL2L2 and miR-26b. Flow cytometry and MTT assay were also performed to observe the effect of MIAT/miR-26b/BCL2L2 signalling pathway on the status of cell apoptosis and viability. Results: MIAT functioned as an endogenous competing RNA to sponge miR-26b. In addition, BCL2L2 was identified as a target of miR-26b. Therefore, the expression of miR-26b was obviously suppressed by MIAT or anti-miR-26b, while the mRNA and protein expression of BCL2L2 was up-regulated in the presence of MIAT or anti-miR-26b. Moreover, the positive effect of MIAT on BCL2L2 expression was exerted via inhibition of the expression of miR-26b. In addition, the cells transfected with MIAT or anti-miR-26b showed suppressed expression of caspase-3 and reduced apoptosis index but higher cell viability, indicating that MIAT could suppress cell apoptosis via inhibition of miR-26b expression. Furthermore, the subjects carrying the GT and TT genotypes of single-nucleotide polymorphism (SNP) rs1894720 were associated with a higher risk of age-related cataracts, as indicated by their odds ratio (OR) and p values. Conclusions: Rs1894720 SNP could down-regulate the expression of MIAT, thus leading to reduced BCL2L2 expression and enhanced epithelial cell apoptosis in the lens, eventually increasing the incidence of age-related cata ract.

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“…Taken together, this evidence could depict a novel molecular paradigm underlying the pathogenesis of 8q24 rearrangement-positive MM. PVT1 knockdown in MM cell lines inhibited cell proliferation and promoted apoptosis [48] through restoration of expression of miR-203a [68] (Fig. 3).…”

Section: Multiple Myelomamentioning

confidence: 93%

“…Elevated PVT1 levels were detected in MM BM cells compared with normal tissue [68] and primarily in MYCrearranged MM cases [69]. In particular, high PVT1 was associated with MM carrying recurrent MYC fusion genes (with IGH, IGK, IGL, TXNDC5/BMP6, FOXO3 and FAM46C partner genes) or complex rearrangements involving more than five loci, or hyperdiploid cases, that also overexpressed MYC [69].…”

Section: Multiple Myelomamentioning

confidence: 96%

“…Indeed, binding sites for EIF4A3, U2AF65, AGO2, AUF1, DGCR8, FUS, HNRNPC, PTB, TAF15, TDP43, TIA1, TIAL1, LIN28A were predicted on circPVT1, with the first 3 RBPs showing the strongest evidence (https://circinteractome.nia.nih.gov/index.html). Among the micro-RNAs regulated by PVT1, miR-26b, miR-203a, miR-214, miR-424 and miR-497 were reported to be deregulated and play a role in the pathogenesis of lymphoma [103][104][105][106][107][108] and/or MM [68,[109][110][111][112][113] and/or leukemia [114][115][116][117][118][119][120][121]. mir-26b appeared among those showing a significant interaction with the core of PVT1coexpressed transcripts (p ≤ 0.05, mirTarbase, https://amp.…”

Section: Pvt1 and Circpvt1: Myc Partners In Crime And Beyondmentioning

confidence: 99%

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Linear and circular PVT1 in hematological malignancies and immune response: two faces of the same coin

et al. 2020

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Non coding RNAs (ncRNAs) have emerged as regulators of human carcinogenesis by affecting the expression of key tumor suppressor genes and oncogenes. They are divided into short and long ncRNAs, according to their length. Circular RNAs (circRNAs) are included in the second group and were recently discovered as being originated by back-splicing, joining either single or multiple exons, or exons with retained introns. The human Plasmacytoma Variant Translocation 1 (PVT1) gene maps on the long arm of chromosome 8 (8q24) and encodes for 52 ncRNAs variants, including 26 linear and 26 circular isoforms, and 6 microRNAs. PVT1 genomic locus is 54 Kb downstream to MYC and several interactions have been described among these two genes, including a feedback regulatory mechanism. MYC-independent functions of PVT1/circPVT1 have been also reported, especially in the regulation of immune responses. We here review and discuss the role of both PVT1 and circPVT1 in the hematopoietic system. No information is currently available concerning their transforming ability in hematopoietic cells. However, present literature supports their cooperation with a more aggressive and/or undifferentiated cell phenotype, thus contributing to cancer progression. PVT1/circPVT1 upregulation through genomic amplification or rearrangements and/or increased transcription, provides a proliferative advantage to malignant cells in acute myeloid leukemia, acute promyelocytic leukemia, Burkitt lymphoma, multiple myeloma (linear PVT1) and acute lymphoblastic leukemia (circPVT1). In addition, PVT1 and circPVT1 regulate immune responses: the overexpression of the linear form in myeloid derived suppressor cells induced immune tolerance in preclinical tumor models and circPVT1 showed immunosuppressive properties in myeloid and lymphoid cell subsets. Overall, these recent data on PVT1 and circPVT1 functions in hematological malignancies and immune responses reflect two faces of the same coin: involvement in cancer progression by promoting a more aggressive phenotype of malignant cells and negative regulation of the immune system as a novel potential therapy-resistance mechanism.

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Down-regulation of miR-203a by lncRNA PVT1 in multiple myeloma promotes cell proliferation

Cited by 42 publications

References 19 publications

Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Tongue Squamous Cell Carcinoma

Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Tongue Squamous Cell Carcinoma

Rs1894720 polymorphism is associated with the risk of age-related cataract by regulating the proliferation of epithelial cells in the lens via the signalling pathway of MIAT/miR-26b/BCL2L2

Linear and circular PVT1 in hematological malignancies and immune response: two faces of the same coin

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