miR-301 regulates the SIRT1/SOX2 pathway via CPEB1 in the breast cancer progression

Jia, Yanjing; Zhao, Jie; Yang, Jinjie; Shao, Jie; Cai, Zihao

doi:10.1016/j.omto.2021.03.007

Cited by 12 publications

(9 citation statements)

References 34 publications

(45 reference statements)

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“…By inhibiting p53 [43] or promoting the activity of PI3K/Akt signaling pathway [44], SIRT1 enhanced proliferation of BC cells. In nude mice models, miR-301 overexpression accelerates the progression of BC by mediating the SIRT1/SOX2 pathway [45]. Additionally, SIRT1 plays a pivotal role in the regulation of the epithelial-mesenchymal transition (EMT) process, which contributes to the metastasis of cancer cells.…”

Section: Discussionmentioning

confidence: 99%

The prognostic implications of SIRTs expression in breast cancer: a systematic review and meta-analysis

Zhang

Peng

et al. 2022

Discov Onc

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Background Sirtuins (SIRTs) have key roles in cancer progression. However, the prognostic implications of SIRTs in breast cancer (BC) remains a subject of debate and controversy. Thus, we performed a meta-analysis to identify the precise prognostic value of SIRTs in BC patients. Methods Systematic literature searching was conducted in PubMed, Cochrane Library, Web of Science, and Embase databases. The pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated to estimate the association of SIRTs expression and survival outcomes in BC patients. Results A total of 22 original studies with 6317 patients were eligible for this meta-analysis. The results showed that in patients with BC, elevated SIRTs levels were associated with shorter overall survival (OS) and disease-free survival (DFS) both in univariate (HR = 1.56, 95% CI 1.21–2.00; HR = 1.67, 95% CI 1.32–2.12, respectively) and multivariate analysis models (HR = 2.11, 95% CI 1.48–3.00; HR = 1.70, 95% CI 1.20–2.39, respectively). Notably, further subgroup analysis revealed that overexpression of SIRT1 and SIRT6 predicted poor OS (HR = 2.65, 95% CI 1.54–4.56; HR = 2.53, 95% CI 1.64–3.90, respectively) and DFS (HR = 1.65, 95% CI 1.07–2.56; HR = 2.74; 95% CI 1.88–4.01, respectively) in BC. Conclusions Our data has elucidated that SIRT1 and SIRT6 could serve as prognostic biomarkers for patients with BC and may contribute to refined patient management.

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Section: Discussionmentioning

confidence: 99%

The prognostic implications of SIRTs expression in breast cancer: a systematic review and meta-analysis

Zhang

Peng

et al. 2022

Discov Onc

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“…1,21,35,36 Its inhibitory effect against apoptosis has been reported in a range of cancers, including breast cancer, ovarian cancer, and prostate cancer. 22,31,37 miRNAs are believed to exert their functional effects by targeting genes using distinctive signalling pathways that have already been implicated in cancers. We previously reported on COM involvement for different KEGG pathways, including the JAK-STAT, NF-kB, MAPK, PI3K-AKT, and AMPK signalling pathways, based on miRNA or transcriptomic profiles.…”

Section: Discussionmentioning

confidence: 99%

“…Among these miRNAs, miR‐301a is upregulated in many cancers and is reportedly responsible for promoting cell migration and proliferation and inhibiting apoptosis 14–24 . Indeed, we previously identified miR‐301a as one of the aberrantly expressed miRNAs in COM, when tissues were screened using next‐generation sequencing 12 .…”

Section: Introductionmentioning

confidence: 99%

“…3,12,13 Among these miRNAs, miR-301a is upregulated in many cancers and is reportedly responsible for promoting cell migration and proliferation and inhibiting apoptosis. [14][15][16][17][18][19][20][21][22][23][24] Indeed, we previously identified miR-301a as one of the aberrantly expressed miRNAs in COM, when tissues were screened using next-generation sequencing. 12 Although the functional roles of miR-301a have been explored in human malignant melanoma, 1 its role in COM is unclear and requires further detailed investigation.…”

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confidence: 99%

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Elevated expression of miR‐301a and its functional roles in canine oral melanoma

Hasan,

Rahman,

Husna

et al. 2023

Vet Comparative Oncology

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AbstractmiR‐301a is one of numerous dysregulated microRNAs (miRNAs) in canine oral melanoma (COM), one of which is miR‐301a (upregulated). Its biological role has been described in various human cancer types, including malignant melanoma, but not in COM. Accordingly, in this study, we investigated miR‐301a expression in COM in greater detail to ascertain whether it could serve as a diagnostic biomarker, elucidate its functional roles in this cancer, and predict the possible pathways by which it exerts its effects. Relative expression of miR‐301a was investigated in clinical oral tissue and plasma samples and COM cell (KMeC and LMeC) lines using qRT‐PCR. Knockdown of miR‐301a was also validated for KMeC and LMeC cells using qRT‐PCR. We performed CCK‐8 assays to assess cell proliferation, monolayer wound‐healing, and transwell migration assays to assess cell migration, a colony‐formation assay to assess clonogenicity, a TUNEL assay and flow cytometry to assess apoptosis‐related effects, and gene enrichment analyses to predict possible related pathways. miR‐301a was markedly upregulated in COM oral tissue and plasma clinically, suggesting its potential as a diagnostic biomarker for COM diagnosis. In vitro assays demonstrated that miR‐301 significantly inhibited apoptosis in COM cells while promoting cell migration, proliferation, and clonogenicity. We also predicted that miR‐301 exerts cancer‐promoting effects through the Wnt signalling pathway for COM. Our findings suggest that miR‐301a is a COM oncomiR that regulates several oncogenic phenotypes with the potential to be a diagnostic biomarker.

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“…demonstrated that the HDAC SIRT1 is upregulated in NEPC and showed that overexpressing SIRT1 promotes NEPC lineage plasticity ( 94 ). SIRT1 has been shown to promote upregulation of SOX2 in breast cancer ( 97 ), liver cancer stem cells ( 98 ), and bone marrow-derived mesenchymal stem cells ( 99 ). Thus, it is possible that SOX2 upregulation by SIRT1 may also contribute to NEPC lineage plasticity.…”

Section: The Role Of Epigenetic Change In Nepc Lineage Plasticitymentioning

confidence: 99%

The Role of Epigenetic Change in Therapy-Induced Neuroendocrine Prostate Cancer Lineage Plasticity

et al. 2022

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The androgen receptor (AR) signaling pathway is critical for growth and differentiation of prostate cancer cells. For that reason, androgen deprivation therapy with medical or surgical castration is the principal treatment for metastatic prostate cancer. More recently, new potent AR signaling inhibitors (ARSIs) have been developed. These drugs improve survival for men with metastatic castration-resistant prostate cancer (CRPC), the lethal form of the disease. However, ARSI resistance is nearly universal. One recently appreciated resistance mechanism is lineage plasticity or switch from an AR-driven, luminal differentiation program to an alternate differentiation program. Importantly, lineage plasticity appears to be increasing in incidence in the era of new ARSIs, strongly implicating AR suppression in this process. Lineage plasticity and shift from AR-driven tumors occur on a continuum, ranging from AR-expressing tumors with low AR activity to AR-null tumors that have activation of alternate differentiation programs versus the canonical luminal program found in AR-driven tumors. In many cases, AR loss coincides with the activation of a neuronal program, most commonly exemplified as therapy-induced neuroendocrine prostate cancer (t-NEPC). While genetic events clearly contribute to prostate cancer lineage plasticity, it is also clear that epigenetic events—including chromatin modifications and DNA methylation—play a major role. Many epigenetic factors are now targetable with drugs, establishing the importance of clarifying critical epigenetic factors that promote lineage plasticity. Furthermore, epigenetic marks are readily measurable, demonstrating the importance of clarifying which measurements will help to identify tumors that have undergone or are at risk of undergoing lineage plasticity. In this review, we discuss the role of AR pathway loss and activation of a neuronal differentiation program as key contributors to t-NEPC lineage plasticity. We also discuss new epigenetic therapeutic strategies to reverse lineage plasticity, including those that have recently entered clinical trials.

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miR-301 regulates the SIRT1/SOX2 pathway via CPEB1 in the breast cancer progression

Cited by 12 publications

References 34 publications

The prognostic implications of SIRTs expression in breast cancer: a systematic review and meta-analysis

The prognostic implications of SIRTs expression in breast cancer: a systematic review and meta-analysis

Elevated expression of miR‐301a and its functional roles in canine oral melanoma

The Role of Epigenetic Change in Therapy-Induced Neuroendocrine Prostate Cancer Lineage Plasticity

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