Noncoding RNA actions through IGFs and IGF binding proteins in cancer

Kerr, Aidan; Baxter, Robert C.

doi:10.1038/s41388-022-02353-3

Cited by 14 publications

(9 citation statements)

References 110 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies have reported that high levels of blood IGFs are associated with an increased risk of breast cancer [54][55][56][57][58][59]. IGF-binding protein (IGFBP) is one of the key regulators of IGF signaling as it functions as a reservoir of serum IGFs [54][55][56][57]59,60]. Based on these studies, increased levels of circulating IGF-1 and IGFBP3 are considered risk factors for breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Circulating microRNA Biomarker for Detecting Breast Cancer in High-Risk Benign Breast Tumors

Khadka

Nasu

Deng

et al. 2023

IJMS

View full text Add to dashboard Cite

High-risk benign breast tumors are known to develop breast cancer at high rates. However, it is still controversial whether they should be removed during diagnosis or followed up until cancer development becomes evident. Therefore, this study sought to identify circulating microRNAs (miRNAs) that could serve as detection markers of cancers arising from high-risk benign tumors. Small RNA-seq was performed using plasma samples collected from patients with early-stage breast cancer (CA) and high-risk (HB), moderate-risk (MB), and no-risk (Be) benign breast tumors. Proteomic profiling of CA and HB plasma was performed to investigate the underlying functions of the identified miRNAs. Our findings revealed that four miRNAs, hsa-mir-128-3p, hsa-mir-421, hsa-mir-130b-5p, and hsa-mir-28-5p, were differentially expressed in CA vs. HB and had diagnostic power to discriminate CA from HB with AUC scores greater than 0.7. Enriched pathways based on the target genes of these miRNAs indicated their association with IGF-1. Furthermore, the Ingenuity Pathway Analysis performed on the proteomic data revealed that the IGF-1 signaling pathway was significantly enriched in CA vs. HB. In conclusion, these findings suggest that these miRNAs could potentially serve as biomarkers for detecting early-stage breast cancer from high-risk benign tumors by monitoring IGF signaling-induced malignant transformation.

show abstract

Section: Discussionmentioning

confidence: 99%

Circulating microRNA Biomarker for Detecting Breast Cancer in High-Risk Benign Breast Tumors

Khadka

Nasu

Deng

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“…Binding of IGF to the IGF receptor activates PI3K/Akt and ERK signaling leading to cancer cell survival, proliferation, and migration [ 46 ]. Conversely, IGFBP suppresses IGF-related signaling pathways by interrupting the IGF-to-IGF receptor binding [ 47 , 48 ]. In our study, we found that ME treatment upregulated the expression of IGFBP3, the most abundant IGFBP, and downregulated the activation of the PI3K-mTOR signaling pathway ( Figs.…”

Section: Discussionmentioning

confidence: 99%

“…5 and 6 ). According to a study by Kerr et al ., microRNA-10a, levels of which are increased by β-sitosterol, acts through the IGF- and IGFBP-related pathways in cancer [ 48 ]. This suggests that β-sitosterol in ME may play a crucial role in modulating the IGFBP-PI3K pathway in pancreatic cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Mychonastes sp. 246 Suppresses Human Pancreatic Cancer Cell Growth via IGFBP3-PI3K-mTOR Signaling

Jang

Lee

Hong

et al. 2022

J. Microbiol. Biotechnol.

View full text Add to dashboard Cite

Previously, we confirmed that Mychonastes sp. 246 methanolic extract (ME) markedly reduced the viability of BxPC-3 human pancreatic cancer cells. However, the underlying mechanism ME remained unclear. Hence, we attempted to elucidate the anticancer effect of ME on BxPC-3 human pancreatic cancer cells. First, we investigated the components of ME and their cytotoxicity in normal cells. Then, we confirmed the G1 phase arrest mediated growth inhibitory effect of ME using a cell counting assay and cell cycle analysis. Moreover, we found that the migration-inhibitory effect of ME using a Transwell migration assay. Through RNA sequencing, Gene Ontology-based network analysis, and western blotting, we explored the intracellular mechanisms of ME in BxPC-3 cells. ME modulated the intracellular energy metabolism-related pathway by altering the mRNA levels of IGFBP3 and PPARGC1A in BxPC-3 cells and reduced PI3K and mTOR phosphorylation by upregulating IGFBP3 and 4E-BP1 expression. Finally, we verified that ME reduced the growth of three-dimensional (3D) pancreatic cancer spheroids. Our study demonstrates that ME suppresses pancreatic cancer proliferation through the IGFBP3-PI3K-mTOR signaling pathway. This is the first study on the anticancer effect of the ME against pancreatic cancer, suggesting therapeutic possibilities and the underlying mechanism of ME action.

show abstract

“…Noncoding RNAs, including microRNAs (miRs) and lncRNAs, have an impact on IGF/IGF1R pathway activity (reviewed in ( 180 )). MiRs are double-stranded short RNAs that are binding to the 3’-upstream region (UTR) of mRNAs to block their translation or to induce their degradation ( 181 ).…”

Section: Regulation Of Igfbp5 Expressionmentioning

confidence: 99%

Biological effects and regulation of IGFBP5 in breast cancer

Dittmer

2022

Front. Endocrinol.

View full text Add to dashboard Cite

The insulin-like growth factor receptor (IGF1R) pathway plays an important role in cancer progression. In breast cancer, the IGF1R pathway is linked to estrogen-dependent signaling. Regulation of IGF1R activity is complex and involves the actions of its ligands IGF1 and IGF2 and those of IGF-binding proteins (IGFBPs). Six IGFBPs are known that share the ability to form complexes with the IGFs, by which they control the bioavailability of these ligands. Besides, each of the IGFBPs have specific features. In this review, the focus lies on the biological effects and regulation of IGFBP5 in breast cancer. In breast cancer, estrogen is a critical regulator of IGFBP5 transcription. It exerts its effect through an intergenic enhancer loop that is part of the chromosomal breast cancer susceptibility region 2q35. The biological effects of IGFBP5 depend upon the cellular context. By inhibiting or promoting IGF1R signaling, IGFBP5 can either act as a tumor suppressor or promoter. Additionally, IGFBP5 possesses IGF-independent activities, which contribute to the complexity by which IGFBP5 interferes with cancer cell behavior.

show abstract

Noncoding RNA actions through IGFs and IGF binding proteins in cancer

Cited by 14 publications

References 110 publications

Circulating microRNA Biomarker for Detecting Breast Cancer in High-Risk Benign Breast Tumors

Circulating microRNA Biomarker for Detecting Breast Cancer in High-Risk Benign Breast Tumors

Mychonastes sp. 246 Suppresses Human Pancreatic Cancer Cell Growth via IGFBP3-PI3K-mTOR Signaling

Biological effects and regulation of IGFBP5 in breast cancer

Contact Info

Product

Resources

About