Secreted microRNAs in bone metastasis

Taipaleenmäki, Hanna

doi:10.1007/s00774-023-01424-z

Cited by 4 publications

(2 citation statements)

References 46 publications

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“…A key aspect in understanding the process of bone metastasis is the recognition of the significant impact of the ‘vicious cycle’. This cycle involves the reciprocal interactions between tumor cells and bone-residing cells, such as osteoblasts and osteoclasts, resulting in both bone degradation and tumor development [ 5 , 6 , 7 ]. This review focuses on analyzing the impact of both local and systemic variables, such as cytokines and growth factors, as well as the metabolic reprogramming of cancer cells and bones on the advancement of bone metastases.…”

Section: Introductionmentioning

confidence: 99%

Bridging the Gap in Understanding Bone Metastasis: A Multifaceted Perspective

Elaasser,

Arakil,

Mohammad

2024

IJMS

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The treatment of patients with advanced cancer poses clinical problems due to the complications that arise as the disease progresses. Bone metastases are a common problem that cancer patients may face, and currently, there are no effective drugs to treat these individuals. Prostate, breast, and lung cancers often spread to the bone, causing significant and disabling health conditions. The bone is a highly active and dynamic tissue and is considered a favorable environment for the growth of cancer. The role of osteoblasts and osteoclasts in the process of bone remodeling and the way in which their interactions change during the progression of metastasis is critical to understanding the pathophysiology of this disease. These interactions create a self-perpetuating loop that stimulates the growth of metastatic cells in the bone. The metabolic reprogramming of both cancer cells and cells in the bone microenvironment has serious implications for the development and progression of metastasis. Insight into the process of bone remodeling and the systemic elements that regulate this process, as well as the cellular changes that occur during the progression of bone metastases, is critical to the discovery of a cure for this disease. It is crucial to explore different therapeutic options that focus specifically on malignancy in the bone microenvironment in order to effectively treat this disease. This review will focus on the bone remodeling process and the effects of metabolic disorders as well as systemic factors like hormones and cytokines on the development of bone metastases. We will also examine the various therapeutic alternatives available today and the upcoming advances in novel treatments.

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Section: Introductionmentioning

confidence: 99%

Bridging the Gap in Understanding Bone Metastasis: A Multifaceted Perspective

Elaasser,

Arakil,

Mohammad

2024

IJMS

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“…They have been linked to the development of many diseases, including various cancers, cardiovascular diseases, and neurodegenerative diseases 2 . For instance, certain miRNAs have been associated with liver cancer, breast cancer 3 , and ovarian cancer 4 , while lncRNAs have been shown to be linked to cardiovascular diseases 5 , diabetes 2 , and breast cancer 6 . RNA methylation is another important area of epigenetic research, and it involves chemical modifications to RNA molecules that can interfere with their interactions with other molecules.…”

Section: Introductionmentioning

confidence: 99%

A comprehensive epigenetic network can influence the occurrence of thyroid-associated ophthalmopathy by affecting immune and inflammatory response

Zhang,

Wu,

Gong

et al. 2024

Sci Rep

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The primary objective of this study is to understand the regulatory role of epigenetics in thyroid-associated ophthalmopathy (TAO) using multi-omics sequencing data. We utilized tRFs sequencing data, DNA methylation sequencing data, and lncRNA/circRNA/mRNA sequencing data, as well as several RNA methylation target prediction websites, to analyze the regulatory effect of DNA methylation, non-coding RNA, and RNA methylation on TAO-associated genes. Through differential expression analysis, we identified 1019 differentially expressed genes, 985 differentially methylated genes, and 2601 non-coding RNA. Functional analysis showed that differentially expressed genes were mostly associated with the PI3K signaling pathway and the IL17 signaling pathway. Genes regulated by DNA epigenetic regulatory networks were mainly related to the Cytokine-cytokine receptor interaction pathway, whereas genes regulated by RNA epigenetic regulatory networks were primarily related to the T cell receptor signaling pathway. Finally, our integrated regulatory network analysis revealed that epigenetics mainly impacts the occurrence of TAO through its effects on key pathways such as cell killing, cytokine production, and immune response. In summary, this study is the first to reveal a new mechanism underlying the development of TAO and provides new directions for future TAO research.

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HTLV-1 infected T cells cause bone loss via small extracellular vesicles

Pokhrel,

Panfil,

Habib

et al. 2024

Preprint

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Adult T cell leukemia (ATL), caused by infection with human T cell leukemia virus type 1 (HTLV-1), is often complicated by hypercalcemia and osteolytic lesions. Therefore, we studied the communication between patient-derived ATL cells (ATL-PDX) and HTLV-1 immortalized CD4+ T cell lines (HTLV/T) with osteoclasts and their effects on bone mass in mice. Intratibial inoculation of some HTLV/T lead to a profound local decrease in bone mass similar to marrow-replacing ATL-PDX, despite the fact that few HTLV/T cells persisted in the bone. To study the direct effect of HTLV/T and ATL-PDX on osteoclasts, supernatants were added to murine and human osteoclast precursors. ATL-PDX supernatants from hypercalcemic patients promoted formation of mature osteoclasts, while those from HTLV/T were variably stimulatory, but had largely consistent effects between human and murine cultures. Interestingly, this osteoclastic activity did not correlate with expression of osteoclastogenic cytokine RANKL, suggesting an alternative mechanism. HTLV/T and ATL-PDX produce small extracellular vesicles (sEV), known to facilitate HTLV-1 infection. We hypothesized that these sEV also mediate bone loss by targeting osteoclasts. We isolated sEV from both HTLV/T and ATL-PDX, and found they carried most of the activity found in supernatants. In contrast, sEV from uninfected activated T cells had little effect. Analysis of sEV (both active and inactive) by mass spectrometry and electron microscopy confirmed absence of RANKL and intact virus. Viral proteins Tax and Env were only present in sEV from the active, osteoclast-stimulatory group, along with increased representation of proteins involved in osteoclastogenesis and bone resorption. sEV injected over mouse calvaria in the presence of low dose RANKL caused more osteolysis than RANKL alone. Thus, HTLV-1 infection of T cells can cause release of sEV with strong osteolytic potential, providing a mechanism beyond RANKL production that modifies the bone microenvironment, even in the absence of overt leukemia.

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Secreted microRNAs in bone metastasis

Cited by 4 publications

References 46 publications

Bridging the Gap in Understanding Bone Metastasis: A Multifaceted Perspective

Bridging the Gap in Understanding Bone Metastasis: A Multifaceted Perspective

A comprehensive epigenetic network can influence the occurrence of thyroid-associated ophthalmopathy by affecting immune and inflammatory response

HTLV-1 infected T cells cause bone loss via small extracellular vesicles

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