MicroRNA expression profile during different conditions of hypoxia

Lacedonia, Donato; Scioscia, Giulia; Palladino, Grazia Pia; Gallo, Crescenzio; Carpagnano, Giovanna Elisiana; Sabato, Roberto; Barbaro, Maria Pia Foschino

doi:10.18632/oncotarget.26210

Cited by 23 publications

(14 citation statements)

References 26 publications

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“…In addition, lncRNAs are often found to cooperate with miRNAs to regulate biological progression in transcription level [15]. miR-145 is often used in various inflammatory progressions in Asthma as well as in chronic obstructive pulmonary disease (COPD) [16]. Is there possible that miR-145 was also involved in OSAHS?…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA ROR mitigates cobalt chloride-induced hypoxia injury through regulation of miR-145

Ge¹,

Liu²,

Liu³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Obstructive sleep apnoea-hypopnoea syndrome (OSAHS) is a condition causing apnea and hypopnea. LncRNA-ROR revealed properties in regulating hypoxia response. Our study explored the roles of ROR in CoCl 2-induced hypoxia injury in HK-2 cells. HK-2 cells were treated with CoCl 2 to induce hypoxia injury. Cell viability, cell apoptosis and apoptotic proteins were detected using CCK-8, flow cytometry and western blot, respectively. The alter expression of ROR and miR-145 was achieved through transfection. Moreover, the expressions of HIF-a and ERK and MAPK related factors were examined using western blot. We found that CoCl 2 decreased cell viability and increased apoptosis as well as increased the expression of ROR. ROR overexpression increased cell viability, decreased cell apoptosis. ROR overexpression upregulated anti-apoptotic proteins Bcl-2 and decreased p53, Bax and cleaved-Caspase-3. ROR overexpression also increased the expression of HIF-a. On the opposite, ROR silence led to the opposite results as relative to ROR overexpression. ROR overexpression decreased expression of miR-145. Co-transfection with ROR overexpression and miR-145 impaired the promoting effects of ROR in CoCl 2 treated cells. ROR increased phosphorylation of ERK while decreased phosphorylation of MAPK. In conclusion, lncRNA ROR alleviated CoCl 2-induced hypoxia injury through regulation of miR-145 as well as modulating ERK and MAPK signalling. HIGHLIGHTS 1. CoCl 2 induces ROR upregulation; 2. Overexpression of ROR reduces CoCl 2-induced HK-2 cell injury; 3. Silence of ROR promotes CoCl 2-induced HK-2 cell injury; 4. Overexpression of ROR decreases miR-145 expression; 5. ROR overexpression modulates ERK and MAPK signalling pathways through regulation of miR-145.

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Section: Introductionmentioning

confidence: 99%

Long non-coding RNA ROR mitigates cobalt chloride-induced hypoxia injury through regulation of miR-145

Ge¹,

Liu²,

Liu³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…The relevance of microenvironment in OSA-induced colorectal carcinogenesis has been recently pointed out by Gao et al, who suggested that intermittent hypoxia, chronic inflammation, and intestinal microbiota dysbiosis cooperate in CRC carcinogenesis in response to OSA [ 20 ]. Intermittent hypoxia influences also the expression of miRNAs, and some of them are known to be involved in cancer development or progression [ 21 ]. Finally, sleep fragmentation represents another factor influencing tumor initiation/progression since it causes epigenetic modifications of many circadian genes, which modify the expression of cancer-related susceptibility genes involved in cell division and DNA repair [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Obstructive Sleep Apnea Worsens Progression-Free and Overall Survival in Human Metastatic Colorectal Carcinoma

Lacedonia

Landriscina

Scioscia

et al. 2021

Journal of Oncology

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Sleep disorders have emerged as highly prevalent conditions, and along with improved understanding of such disorders, increased attention has gained the evidence that perturbation in sleep architecture and continuity may initiate, exacerbate, or modulate the phenotypic expression of multiple diseases including cancer. Furthermore, obstructive sleep apnea (OSA) has recently been implicated in increased incidence and more adverse prognosis of cancer in humans. This study was designed to confirm the high prevalence of OSA in human malignancies and assess its prognostic relevance in metastatic colorectal carcinomas (mCRCs). A prospective cohort of 52 subjects, affected by solid histologically confirmed metastatic malignancies, was analyzed, and among them, 29 mCRCs were studied for the prognostic role of OSA. OSA was diagnosed in 34.6% (18/52) of patients with a statistically significant difference in apnea-hyponea index between OSA and non-OSA subgroups (14.2 ± 12.2 vs. 2.1 ± 1.5, p < 0.01 ). Consistently, OSA was diagnosed in 34.5% (10/29) of mCRCs with lower rates of first-line therapy disease control in OSA compared to non-OSA patients (60% in OSA vs. 94.7% in non-OSA, p = 0.03 ). Of note, progression-free and overall survival rates were significantly shorter in OSA (respectively, 9 and 22 months) compared non-OSA (20 and 40 months) mCRC patients (HR = 2.63; 95% CI 0.88–7.84, p = 0.01 for PFS; HR = 3.93; 95% CI 1.13–13.73, p < 0.001 for OS). Finally, the multivariate analysis showed that OSA is an independent prognostic factor for PFS p = 0.0076 and OS p = 0.0017 in this cohort. Altogether, these data suggest that OSA is a potential clinical marker predictor of poor prognosis in patients with mCRC.

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“…Therefore, the underlying mechanisms in the IH-induced increase of epiregulin remain unclear and are very attractive areas for future research to establish prophylaxis for cardiovascular diseases in patients with OSA. Recently, there has been increased evidence that IH induces changes in microRNA expression in several types of cells in patients with sleep disorders [92,93,94,95], and therefore microRNAs may play pivotal roles in cellular responses to IH, including the increase of epiregulin expression in VSMCs.…”

Section: Epiregulinmentioning

confidence: 99%

Proliferative Pathways of Vascular Smooth Muscle Cells in Response to Intermittent Hypoxia

Kyotani

Takasawa

Yoshizumi

2019

IJMS

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Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH) and is a risk factor for cardiovascular diseases (e.g., atherosclerosis) and chronic inflammatory diseases (CID). The excessive proliferation of vascular smooth muscle cells (VSMCs) plays a pivotal role in the progression of atherosclerosis. Hypoxia-inducible factor-1 and nuclear factor-κB are thought to be the main factors involved in responses to IH and in regulating adaptations or inflammation pathways, however, further evidence is needed to demonstrate the underlying mechanisms of this process in VSMCs. Furthermore, few studies of IH have examined smooth muscle cell responses. Our previous studies demonstrated that increased interleukin (IL)-6, epidermal growth factor family ligands, and erbB2 receptor, some of which amplify inflammation and, consequently, induce CID, were induced by IH and were involved in the proliferation of VSMCs. Since IH increased IL-6 and epiregulin expression in VSMCs, the same phenomenon may also occur in other smooth muscle cells, and, consequently, may be related to the incidence or progression of several diseases. In the present review, we describe how IH can induce the excessive proliferation of VSMCs and we develop the suggestion that other CID may be related to the effects of IH on other smooth muscle cells.

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MicroRNA expression profile during different conditions of hypoxia

Cited by 23 publications

References 26 publications

Long non-coding RNA ROR mitigates cobalt chloride-induced hypoxia injury through regulation of miR-145

Long non-coding RNA ROR mitigates cobalt chloride-induced hypoxia injury through regulation of miR-145

Obstructive Sleep Apnea Worsens Progression-Free and Overall Survival in Human Metastatic Colorectal Carcinoma

Proliferative Pathways of Vascular Smooth Muscle Cells in Response to Intermittent Hypoxia

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