<i>Retracted:</i> Decreased expression of long noncoding RNA XLOC_013703 promotes cell growth via NF‐κB pathway in multiple myeloma

Pu, Jun; Huang, Hongming; Su, Jianyou; Yuan, Jie; Cong, Hui; Wang, Xudong; Ju, Shaoqing

doi:10.1002/iub.2029

Cited by 11 publications

(13 citation statements)

References 37 publications

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“…Abnormal expression of lncRNAs contribute to the tumorigenesis and development of MM, and can act as valuable diagnosis markers and attractive therapeutic targets for MM [13,14]. In the present study, SNHG16 expression was markedly increased in tissue from MM patients.…”

Section: Discussionsupporting

confidence: 55%

Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p

et al. 2020

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Background: Aberrant expression of long non-coding RNAs (lncRNAs) is closely associated with development and prognosis of human cancers. LncRNA SNHG16 is reportedly involved in human cancer; however, its roles in multiple myeloma (MM) remain unclear. Methods: In this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR. Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16. Results: SNHG16 expression was up-regulated in MM tissues. SNHG16 knockdown suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted the apoptosis of MM cells. Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression. Conclusion: Knockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG16 as a novel therapeutic target for MM.

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Section: Discussionsupporting

confidence: 55%

Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p

et al. 2020

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“…Decreased lncRNA XLOC_013703 enhances cell growth through a nuclear factor-κB pathway in MM. 22 LncRNA NR_046683 acts as a prognostic biomarker and reliable drug target in MM. 23 Nevertheless, the molecular mechanisms of specific lncRNAs in MM are still needed to be deeply inquired.…”

Section: Fut4 Overexpression Reversed the Hoxb-as1 Inhibition-reprementioning

confidence: 99%

LncRNA HOXB‐AS1 promotes cell growth in multiple myeloma via FUT4 mRNA stability by ELAVL1

Chen

Zhang

Wang

2019

J of Cellular Biochemistry

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Multiple myeloma (MM) is defined as the second most common hematological tumor in the globe. Long noncoding RNAs (lncRNAs) have been reported to play stimulative or suppressive role in the progression of different carcinomas. The investigation of lncRNAs in MM is still inadequate. LncRNA HOXB cluster antisense RNA 1 (HOXB‐AS1) was once revealed to facilitate glioma progression by affecting cellular activities of glioma cells. However, whether HOXB‐AS1 participates in the development of MM still remains an enigma. In this study, we unveiled that HOXB‐AS1 was highly expressed in MM and loss‐of‐function assays certified that HOXB‐AS1 obstruction suppressed MM cell proliferation, and stimulated cell apoptosis. In addition, HOXB‐AS1 could modulate fucosyltransferase 4 (FUT4) and FUT4‐mediated Wnt/β‐catenin pathway. In subsequence, it was observed from mechanism assays that HOXB‐AS1 enhanced the interaction between ELAVL1 and FUT4 so as to stabilize FUT4 messenger RNA. In the end, rescue experiments affirmed that HOXB‐AS1 affected the cell growth through FUT4 in MM. In conclusion, the whole modulation mechanism of HOXB‐AS1/ELAVL1/FUT4 axis in MM was validated in this study, which suggested that HOXB‐AS1 might function as a powerful and promising therapeutic biomarker for the clinical treatment of patients with MM.

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“…There still exist some deficiencies in our investigation. Signal pathways associated with the evolvement of MM, like NF-κB pathway [9], PI3K/AKT pathway [34] and TGF-β/Smad pathway [35], would to be investigated to figure out whether they were involved in the lncRNA OIP5-AS1-mediated or miR-27a-3p-mediated MM progression.…”

Section: Discussionmentioning

confidence: 99%

“…High expression of lncRNA small nucleolar RNA host gene 18 (SNHG18) and semaphorin 5A (SEMA5A) could indicate unfavorable prognosis of patients with MM [8]. In addition, lncRNA XLOC_013703 modulated survival and proliferation of MM cells through nuclear factor-κB pathway, functioning as a potential therapy target for MM [9]. LncRNA opa interacting protein 5-antisense 1 (OIP5-AS1) could facilitate complicated cellular mechanisms in the development of human malignant tumors [10].…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA OIP5-AS1 suppresses multiple myeloma progression by sponging miR-27a-3p to activate TSC1 expression

Wang

Ruan

et al. 2020

Cancer Cell Int

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Background: Multiple myeloma (MM) is a prevalent hematological malignancy. Long noncoding RNAs are correlated with the development of MM. In this project, the function of lncRNA opa interacting protein 5-antisense 1 (OIP5-AS1) in MM and the potential mechanistic pathway were explored. Methods: The expression of OIP5-AS1, microRNA (miR)-27a-3p and tuberous sclerosis 1 (TSC1) was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) assay. Cell proliferation was assessed by Cell Counting Kit-8 (CCK-8) assay, colony formation assay and Bromodeoxyuridine (BrdU) staining. And cell apoptosis was evaluated by flow cytometry assay. Cell metastasis was assessed utilizing transwell assay. Western blot analysis was employed to detect protein level. The target relation between miR-27a-3p and OIP5-AS1 or TSC1 was confirmed via dual-luciferase reporter assay and RNA immunoprecipitation assay. Tumor xenograft assay was conducted to measure the function of OIP5-AS1 in vivo. Results: The expression levels of OIP5-AS1 and TSC1 were decreased in MM, whereas miR-27a-3p was upregulated. High level of OIP5-AS1 could predict favourable prognosis of MM patients. Overexpression of OIP5-AS1 inhibited cell viability, colony formation ability, migration and invasion, induced cell cycle arrest in G1 phase and apoptosis of MM cells in vitro as well as repressed tumorigenesis in vivo. MiR-27a-3p was a target of OIP5-AS1, and reversed the impact of OIP5-AS1 on MM cells. MiR-27a-3p directly targeted TSC1. Silencing of miR-27a-3p repressed MM progression by elevating TSC1 expression. OIP5-AS1 upregulated TSC1 by sponging miR-27a-3p. Conclusion: OIP5-AS1 repressed multiple myeloma progression by regulating miR-27a-3p/TSC1 axis.

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Retracted: Decreased expression of long noncoding RNA XLOC_013703 promotes cell growth via NF‐κB pathway in multiple myeloma

Cited by 11 publications

References 37 publications

Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p

Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p

LncRNA HOXB‐AS1 promotes cell growth in multiple myeloma via FUT4 mRNA stability by ELAVL1

Long non-coding RNA OIP5-AS1 suppresses multiple myeloma progression by sponging miR-27a-3p to activate TSC1 expression

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