miR-26b-5p suppresses proliferation and promotes apoptosis in multiple myeloma cells by targeting JAG1

Jia, Chuiming; Tian, Yuzhou; Quan, Lina; Jiang, Li; Liu, Ai-Chun

doi:10.1016/j.prp.2018.07.025

Cited by 41 publications

(30 citation statements)

References 20 publications

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“…In the recent years several studies supported the hypothesis that the development of resistance to such treatment is strongly dependent upon the BM microenvironment, with a significant contribution of the CXCR4/SDF1α axis (32)(33)(34) (11,13). Moreover, the activation of Notch signaling in MM cells, induced by tumor cell- (37,38) or BMSC-derived Jagged1 (25), stimulates MM cells proliferation (38), resistance to apoptosis (37) and decrease of drug sensitivity (25).…”

Section: Jagged1 and Jagged2 Blockade Promotes Sensitivity To Bortezomentioning

confidence: 96%

Multiple myeloma exploits Jagged1 and Jagged2 to promote intrinsic and bone marrow-dependent drug resistance

et al. 2019

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Section: Jagged1 and Jagged2 Blockade Promotes Sensitivity To Bortezomentioning

confidence: 96%

Multiple myeloma exploits Jagged1 and Jagged2 to promote intrinsic and bone marrow-dependent drug resistance

et al. 2019

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“…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%

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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“…In the past few decades, a large number of miRNAs have been reported to act as modulators of cancer pathogenesis (in malignancies such as lung and ovarian cancer) (20,21). In MM, several miRNAs have been reported to exert anti-cancerous functions (22,23). Wu et al (22) observed that miR-203 suppressed MM cell proliferation and regulated G 1 /S transition by targeting Bmi-1.…”

Section: Univariate Cox Regression Multivariate Cox Regression ------mentioning

confidence: 99%

“…Wu et al (22) observed that miR-203 suppressed MM cell proliferation and regulated G 1 /S transition by targeting Bmi-1. Jia et al (23) demonstrated that miR-26b inhibited cellular proliferation and induced apoptosis by targeting Jagged1 in MM cells. These studies indicate that miRNAs serve crucial roles in inhibiting the progression Figure 5.…”

Section: Univariate Cox Regression Multivariate Cox Regression ------mentioning

confidence: 99%

“…of MM. Considering that miR-203 and miR-26b play supressive roles in MM development, and in addition to miR-643, are predicted targets of lnc-TCF7 (22,23), the present study aimed to determine whether lnc-TCF7 reversely mediated these three miRNAs by evaluating their expression following lnc-TCF-knockdown. The data showed that lnc-TCF7-knockdown stimulated miR-203 expression but did not affect that of miR-26b or miR-643, suggesting that lnc-TCF7 reversely modulated miR-203 expression in MM cells.…”

Section: Univariate Cox Regression Multivariate Cox Regression ------mentioning

confidence: 99%

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lncRNA transcription factor 7 is related to deteriorating clinical features and poor prognosis in multiple myeloma, and its knockdown suppresses disease progression by regulating the miR‑203‑mediated Jagged1‑Notch1 signaling pathway

Liu

Shen

et al. 2021

Oncol Lett

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Multiple myeloma (MM) remains a challenge to treat, and its precise pathogenic mechanisms have not been fully clarified. The present study aimed to evaluate the relation between long non-coding RNA transcription factor 7 (lnc-TCF7) and clinical features, as well as the prognosis of patients with MM, and to determine the effects of lnc-TCF7-knockdown on the regulation (and regulatory mechanisms) of MM progression. lnc-TCF7 expression was detected in the bone marrow plasma cells of 86 patients with MM and 30 healthy controls. In patients with MM, the clinical data were collected, and event-free survival (EFS) and overall survival (OS) analyses were conducted. In vitro, lnc-TCF7 expression was detected in MM cell lines and normal bone marrow plasma cells. Using Roswell Park Memorial Institute 8226 cells, functional experiments were conducted following lnc-TCF7 short hairpin (sh)RNA transfection, and compensation experiments were performed after lnc-TCF7 shRNA transfection alone and in combination with a microRNA (miR)-203 inhibitor. lnc-TCF7 expression was increased in patients with MM compared with the healthy controls and was positively related to β-2-microglobulin expression and International Staging System stage, while negatively associated with complete response, EFS and OS. In vitro, lnc-TCF7 was upregulated in MM cells compared with normal bone marrow plasma cells, and its knockdown suppressed MM cell proliferation while promoting apoptosis. Compensation experiments showed that miR-203 inhibition promoted MM progression by regulating the Jagged1-Notch1 signaling pathway in lnc-TCF7-knockdown cells. In conclusion, increased lnc-TCF7 expression was related to deteriorating clinical features and prognosis, and lnc-TCF7-knockdown inhibited disease progression by regulating the miR-203-mediated Jagged1-Notch1 signaling pathway activation in MM.

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miR-26b-5p suppresses proliferation and promotes apoptosis in multiple myeloma cells by targeting JAG1

Cited by 41 publications

References 20 publications

Multiple myeloma exploits Jagged1 and Jagged2 to promote intrinsic and bone marrow-dependent drug resistance

Multiple myeloma exploits Jagged1 and Jagged2 to promote intrinsic and bone marrow-dependent drug resistance

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

lncRNA transcription factor 7 is related to deteriorating clinical features and poor prognosis in multiple myeloma, and its knockdown suppresses disease progression by regulating the miR‑203‑mediated Jagged1‑Notch1 signaling pathway

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