Biological effects and regulation of IGFBP5 in breast cancer

Dittmer, Jürgen

doi:10.3389/fendo.2022.983793

Cited by 17 publications

(11 citation statements)

References 245 publications

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“…Microarray analysis of nonfunctional pituitary adenomas (comprising mostly gonadotroph PitNETs) shows higher expression of MYO5A and IGFBP5 in invasive forms compared to non-invasive forms [111]. MYO5A and IGFBP5 are involved in tumor cell migration and metastasis in other cancers [112][113][114]. In another study, bulk RNA-seq of gonadotroph PitNETs shows that genes regulating epithelial-mesenchymal transition (i.e., SPAG9, SKIL, MTDH, HOOK1, CNOT6L, and PRKACB) are particularly highly expressed in fast-growing tumors, as measured by tumor volume doubling time.…”

Section: Gonadotroph Pitnets and Null Cell Pitnetsmentioning

confidence: 99%

Transcriptomic Profiles of Normal Pituitary Cells and Pituitary Neuroendocrine Tumor Cells

Osorio

Jung

et al. 2022

Cancers

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The pituitary gland is one of the most cellularly diverse regions of the brain. Recent advancements in transcriptomic biology, such as single-cell RNA sequencing, bring an unprecedented glimpse into the molecular composition of the pituitary, both in its normal physiological state and in disease. Deciphering the normal pituitary transcriptomic signatures provides a better insight into the ontological origin and development of five types of endocrine cells, a process involving complex cascades of transcription factors that are still being established. In parallel with these observations about normal pituitary development, recent transcriptomic findings on pituitary neuroendocrine tumors (PitNETs) demonstrate both preservations and changes in transcription factor expression patterns compared to those seen during gland development. Furthermore, recent studies also identify differentially expressed genes that drive various tumor behaviors, including hormone hypersecretion and tumor aggression. Understanding the comprehensive multiomic profiles of PitNETs is essential in developing molecular profile-based therapies for PitNETs not curable with current treatment modalities and could eventually help align PitNETs with the breakthroughs being made in applying precision medicine to other tumors.

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Section: Gonadotroph Pitnets and Null Cell Pitnetsmentioning

confidence: 99%

Transcriptomic Profiles of Normal Pituitary Cells and Pituitary Neuroendocrine Tumor Cells

Osorio

Jung

et al. 2022

Cancers

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“…We observed significant upregulation of IGFBP5 and JUN in the W0-I subpopulation. Previous studies have implicated IGFBP5 in cancer inhibition by temporally inactivating the insulin-like growth factor receptor [16], and JUN has been linked to increased tamoxifen sensitivity through protein kinase C activation [17, 18]. Conversely, a positive cell cycle regulator CCND1 [19] and apoptosis inhibitor XBP1 [20] were significantly upregulated in W0-II, while other positive cell cycle regulators CCNA2 [21] and CCNB1/2 [22] were significantly upregulated in W0-III ( Figure A1a ).…”

Section: Resultsmentioning

confidence: 99%

Identifying key regulatory genes in drug resistance acquisition: Modeling pseudotime trajectories of single-cell transcriptome

Iida,

Okada

2024

Preprint

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Single-cell RNA-sequencing (scRNA-seq) technology has provided significant insights into cancer drug resistance at the single-cell level. However, understanding dynamic cell transitions at the molecular systems level remains limited, requiring a systems biology approach. We present an approach that combines mathematical modeling with pseudotime analysis using time-series scRNA-seq data obtained from the breast cancer cell line MCF-7 treated with tamoxifen. Our single-cell analysis identified five distinct subpopulations, including tamoxifen-sensitive and -resistant groups. Using a single-gene mathematical model, we discovered approximately 560-680 genes out of 6,000 exhibiting multistable expression states in each subpopulation, including key estrogen receptor-positive breast cancer cell survival genes, such asRPS6KB1. Bifurcation analysis elucidated their regulatory mechanisms, and we mapped these genes into a molecular network associated with cell survival and metastasis-related pathways. Our modeling approach comprehensively identifies key regulatory genes for drug resistance acquisition, enhancing our understanding of potential drug targets in breast cancer.

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“… 11 For instance, linc0255 increases E2 promoter-binding factor 1 (E2F1) translation by interacting with ribosomal protein L35 (RPL35) in MyCN-amplified neuroblastomas, while disrupted in renal carcinoma 3 (DIRC3) affects chromatin structure and enhances transcription of nearby tumor suppressor genes like IGFBP5. 12 (3) Post-transcriptional level regulation. lncRNAs regulate gene expression by binding to mRNA and affecting key processing sites.…”

Section: Structure and Function Of Lncrnamentioning

confidence: 99%

Research Progress of Long Non-Coding RNA in Tumor Drug Resistance: A New Paradigm

Zhang,

Wu,

Wang

et al. 2024

DDDT

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In the past few decades, chemotherapy has been one of the most effective cancer treatment options. Drug resistance is currently one of the greatest obstacles to effective cancer treatment. Even though drug resistance mechanisms have been extensively investigated, they have not been fully elucidated. Recent genome-wide investigations have revealed the existence of a substantial quantity of long non-coding RNAs (lncRNAs) transcribed from the human genome, which actively participate in numerous biological processes, such as transcription, splicing, epigenetics, the cell cycle, cell differentiation, development, pluripotency, immune microenvironment. The abnormal expression of lncRNA is considered a contributing factor to the drug resistance. Furthermore, drug resistance may be influenced by genetic and epigenetic variations, as well as individual differences in patient treatment response, attributable to polymorphisms in metabolic enzyme genes. This review focuses on the mechanism of lncRNAs resistance to target drugs in the study of tumors with high mortality, aiming to establish a theoretical foundation for targeted therapy.

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Biological effects and regulation of IGFBP5 in breast cancer

Cited by 17 publications

References 245 publications

Transcriptomic Profiles of Normal Pituitary Cells and Pituitary Neuroendocrine Tumor Cells

Transcriptomic Profiles of Normal Pituitary Cells and Pituitary Neuroendocrine Tumor Cells

Identifying key regulatory genes in drug resistance acquisition: Modeling pseudotime trajectories of single-cell transcriptome

Research Progress of Long Non-Coding RNA in Tumor Drug Resistance: A New Paradigm

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