MicroRNA‑22 regulates autophagy and apoptosis in cisplatin resistance of osteosarcoma

Meng, Chenyang; Zhao, Zhenqun; Bai, Rui; Zhao, Wei; Yuxing, Wang; Sun, Liang; Sun, Chao; Feng, Wei; Guo, Sisi

doi:10.3892/mmr.2020.11447

Cited by 12 publications

(10 citation statements)

References 41 publications

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“…CDDP combined with advanced surgery is widely used for the treatment of OS, but as drug resistance increases, the prognosis of patients becomes more unfavourable. Numerous noncoding RNAs, such as circRNAs and miRNAs, have been shown to be involved in the development of drug resistance in OS [ 53 , 54 ]. According to in vitro and in vivo studies, overexpression of circPRKAR1B suppressed the resistance of OS cells to CDDP.…”

Section: Discussionmentioning

confidence: 99%

EIF4A3-induced circular RNA PRKAR1B promotes osteosarcoma progression by miR-361-3p-mediated induction of FZD4 expression

et al. 2021

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Emerging evidence indicates that circRNAs are broadly expressed in osteosarcoma (OS) cells and play a crucial role in OS progression. Recently, cancer-specific circRNA circPRKAR1B has been identified by high-throughput sequencing and is recorded in publicly available databases. Nevertheless, the detailed functions and underlying mechanisms of circPRKAR1B in OS remains poorly understood. By functional experiments, we found that circPRKAR1B enhanced OS cell proliferation, migration, and promotes OS epithelial–mesenchymal transition (EMT). Mechanistic investigations suggested that circPRKAR1B promotes OS progression through sponging miR-361-3p to modulate the expression of FZD4. Subsequently, we identified that EIF4A3 promoted cirPRKAR1B formation through binding to the downstream target of circPRKAR1B on PRKAR1B mRNA. Further rescue study revealed that overexpression of the Wnt signalling could impair the onco-suppressor activities of the silencing of circPRKAR1B. Interestingly, further experiments indicated that circPRKAR1B is involved in the sensitivity of chemoresistance in OS. On the whole, our results demonstrated that circPRKAR1B exerted oncogenic roles in OS and suggested the circPRKAR1B/miR-361-3p/FZD4 axis plays an important role in OS progression and might be a potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

EIF4A3-induced circular RNA PRKAR1B promotes osteosarcoma progression by miR-361-3p-mediated induction of FZD4 expression

et al. 2021

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“…Of these, 43 investigated the molecular regulatory mechanisms of lncRNAs in chemotherapeutic drug resistance in OS, 101 focused on miRNAs, 21 on circRNAs, and one study reported on both lncRNA MEG3 and hsa_circ_0001258 ( Zhu et al, 2019 ). Moreover, 19 overlapping ncRNAs were reported in more than one study, including four lncRNAs (lncRNA SNHG15 [ Sun et al, 2022 ; Zhang et al, 2020a ], lncRNA OIP5-AS1 [ Song et al, 2019 ; Liu and Wang, 2020 ; Sun et al, 2020 ; Kun-Peng et al, 2019 ], lncRNA TUG1 [ Zhou et al, 2020 ; Hu et al, 2019 ], and lncRNA ANRIL [ Li and Zhu, 2019b ; Lee et al, 2021 ]), 13 miRNAs (miR-29b [ Luo et al, 2019 ; Li et al, 2020 ], miR-21 [ Vanas et al, 2016 ; Ziyan and Yang, 2016 ], miR-22 [ Wang et al, 2019c ; Li et al, 2014 ; Meng et al, 2020a ; Meng et al, 2020b ; Zhou et al, 2018b ], miR-199a-3p [ Lei et al, 2018 ; Gao et al, 2015 ], miR-34a-5p [ Pu et al, 2016 ; Pu et al, 2017b ; Pu et al, 2017a ], miR-34a [ Li et al, 2017 ; Novello et al, 2014 ; Chen et al, 2016a ], miR-140-5p [ Wei et al, 2016 ; Meng et al, 2017 ], miR-203 [ Chen et al, 2016a ; Huang et al, 2021 ], miR-19a-3p [ Zhang et al, 2019 ; Wang et al, 2022a ], miR-140 [ Song et al, 2009 ; Zhi et al, 2022 ], miR-29 [ Osaki et al, 2016 ; Xu et al, 2018b ], miR-221 [ Yu et al, 2019 ; Zhao et al, 2013 ], and miR-100 [ Xiao et al, 2017 ; Liu et al, 2016 ]), and two circRNAs (circPTV1 [ Li et al, 2021c ; Kun-Peng et al, 2018a ; Wang et al, 2022c ] and circRNA_0004674 [ Ma et al, 2021 ; Bai et al, 2021 ]) (…”

Section: Resultsmentioning

confidence: 99%

Non-coding RNAs in drug and radiation resistance of bone and soft-tissue sarcoma: a systematic review

Chen

Zhang

et al. 2022

eLife

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Background: Sarcomas comprise approximately 1% of all human malignancies; treatment resistance is one of the major reasons for the poor prognosis of sarcomas. Accumulating evidence suggests that non-coding RNAs, including microRNAs, long non-coding RNAs, and circular RNAs, are important molecules involved in the crosstalk between resistance to chemotherapy, targeted therapy, and radiotherapy via various pathways. Methods: We searched the PubMed (MEDLINE) database for articles regarding sarcoma-associated non-coding RNAs from inception to August17, 2022. Studies investigating the roles of host-derived microRNAs, long non-coding RNAs, and circular RNAs in sarcoma were included. Data regarding the roles of ncRNAs in therapeutic regulation and their applicability as biomarkers for predicting therapeutic response of sarcomas were extracted. Two independent researchers assessed the quality of the studies using Würzburg Methodological Quality Score(W-MeQS). Results: Observational studies revealed ectopic expression of non-coding RNAs in sarcoma patients with different responses to antitumor treatments. Experimental studies have confirmed crosstalk between cellular pathways pertinent to chemotherapy, targeted therapy, and radiotherapy resistance. Of the included studies, W-MeQS scores ranged from 3 to 10 (average score = 5.42). Of the twelve articles that investigated non-coding RNAs as biomarkers, none included a validation cohort. Selective reporting of the sensitivity, specificity, and receiver operating curves was common. Conclusion: Although non-coding RNAs appear to be good candidates as biomarkers for predicting treatment response and therapeutics for sarcoma, their differential expression across tissues complicates their application. Further research regarding their potential for inhibiting or activating these regulatory molecules to reverse treatment resistance may be useful. Funding: This study's literature retrieval cost was supported by the 345 Talent Project of Shengjing Hospital of China Medical University(M0949 to Tao Zhang).

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“…It has been well documented that autophagy exerts key roles in increasing CDDP resistance in OS cells [ 34 ]. By contrary, inhibited autophagy is capable of boosting sensitivity of OS cells to CDDP, along with the reduced Beclin1 level and LC3-II/LC3-I ratio [ 35 , 36 ]. In recent years, studies have found that lncRNA-mediated dysregulation of targets and pathways is considered to be the key cause of chemotherapy resistance [ 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

Exosomal CTCF Confers Cisplatin Resistance in Osteosarcoma by Promoting Autophagy via the IGF2-AS/miR-579-3p/MSH6 Axis

Zhan

Xiao

Wang

et al. 2022

Journal of Oncology

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Cancer-derived exosomes participate in carcinogenesis and progression of cancers, including metastasis and drug-resistance. Of note, CTCF has been suggested to induce drug resistance in various cancers. Herein, we aim to investigate the role of cisplatin- (CDDP-) resistant osteosarcoma- (OS-) derived exosomal CTCF in OS cell resistance to CDDP and its mechanistic basis. Differentially expressed transcription factors, long noncoding RNAs (lncRNAs), miRNAs, and genes in OS were retrieved using bioinformatics approaches. Exosomes were extracted from CDDP-resistant OS cells and then cocultured with parental OS cells, followed by lentiviral transduction to manipulate the expression of CTCF, IGF2-AS, miR-579-3p, and MSH6. We assessed the in vitro and in vivo effects on malignant phenotypes, autophagy, CDDP sensitivity, and tumor formation of OS cells. It was established that CTCF and IGF2-AS were highly expressed in CDDP-resistant OS cells, and the CDDP-resistant OS cell-derived exosomal CTCF enhanced IGF2-AS transcription. CDDP-resistant OS-derived exosomes transmitted CTCF to OS cells and increased CDDP resistance in OS cells by activating an autophagy-dependent pathway. Mechanistically, CTCF activated IGF2-AS transcription and IGF2-AS competitively bound to miR-579-3p to upregulate MSH6 expression. Additionally, the promoting function of exosomal CTCF-mediated IGF2-AS/miR-579-3p/MSH6 in OS cell resistance to CDDP was confirmed in vivo. Taken together, CDDP-resistant OS-derived exosomal CTCF enhanced resistance of OS cells to CDDP via activating the autophagy-dependent pathway, providing a potential therapeutic consideration for OS treatment.

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MicroRNA‑22 regulates autophagy and apoptosis in cisplatin resistance of osteosarcoma

Cited by 12 publications

References 41 publications

EIF4A3-induced circular RNA PRKAR1B promotes osteosarcoma progression by miR-361-3p-mediated induction of FZD4 expression

EIF4A3-induced circular RNA PRKAR1B promotes osteosarcoma progression by miR-361-3p-mediated induction of FZD4 expression

Non-coding RNAs in drug and radiation resistance of bone and soft-tissue sarcoma: a systematic review

Exosomal CTCF Confers Cisplatin Resistance in Osteosarcoma by Promoting Autophagy via the IGF2-AS/miR-579-3p/MSH6 Axis

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