miRNA-7062-5p Promoting Bone Resorption After Bone Metastasis of Colorectal Cancer Through Inhibiting GPR65

Chen, Liang; Wang, Yu; Lu, Xiyi; Zhang, Lili; Wang, Ziming

doi:10.3389/fcell.2021.681968

Cited by 5 publications

(5 citation statements)

References 47 publications

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“…miRNA aberrations have been frequently identified in a wide variety of cancers [ 34 ]. For HNSC, previous studies have found 128 miRNAs were differentially expressed in HNSCC tissue in TCGA dataset.…”

Section: Discussionmentioning

confidence: 99%

The Long Noncoding Transcript HNSCAT1 Activates KRT80 and Triggers Therapeutic Efficacy in Head and Neck Squamous Cell Carcinoma

Zhao

Huang

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Head and neck squamous carcinoma (HNSC) is the most prevalent malignancy of the head and neck regions. Long noncoding RNAs (lncRNAs) are vital in tumorigenesis regulation. However, the role of lncRNAs in HNSC requires further exploration. Herein, through bioinformatic assays using The Cancer Genome Atlas (TCGA) datasets, rapid amplification of cDNA ends (RACE) assays, and RNA-FISH, we revealed that a novel cytoplasmic transcript, HNSC-associated transcript 1 (HNSCAT1, previously recognized as linc01269), was downregulated in tumor samples and advanced tumor stages and was also associated with favorable outcomes in HNSC. Overexpression of HNSCAT1 triggered treatment efficacy in HNSCs both in vivo and in vitro. More importantly, through high-throughput transcriptome analysis (RNA-seq, in NODE database, OEZ007550), we identified KRT80, a tumor suppressor in HNSC, as the target of HNSCAT1. KRT80 expression was modulated by lncRNA HNSCAT1 and presented a positive correlation in tumor samples ( R = 0.52 , p < 0.001 ). Intriguingly, we identified that miR-1245 simultaneously interacts with KRT80 and HNSCAT1, which bridges the regulatory function between KRT80 and HNSCAT1. Conclusively, our study demonstrated that lncRNA HNSCAT1 functions as a necessary tumor inhibitor in HNSC, which provides a novel mechanism of lncRNA function and provides alternative targets for the diagnosis and treatment of HNSC.

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Section: Discussionmentioning

confidence: 99%

The Long Noncoding Transcript HNSCAT1 Activates KRT80 and Triggers Therapeutic Efficacy in Head and Neck Squamous Cell Carcinoma

Zhao

Huang

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…In contrast, GPR40/GPR120 inhibit osteoclastogenesis [ 27 ]. Similarly, the downregulation of GPR65 mediated by miR-7062-5p promotes osteoclast formation [ 17 ]. In this study, we found that GPR84 also inhibited osteoclastogenesis in CRC bone metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…In bone metastasis, ovarian cancer GPR1 mediates communication between cancer cells and osteoblast-like cells [ 16 ]. In addition, GPR65 is downregulated in OCPs during bone metastasis of CRC by miR-7062-5p [ 17 ]. Moreover, GPR65/ADGRG1 is upregulated in 4T1 cells, a BC cell line, and in bone metastatic foci of patients with BC [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

GPR84 potently inhibits osteoclastogenesis and alleviates osteolysis in bone metastasis of colorectal cancer

Shi-Wei²,

Jiang³

et al. 2023

J Orthop Surg Res

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The expression of GPR84 in bone marrow-derived monocytes/macrophages (BMMs) can inhibit osteoclast formation; however, its role in bone metastasis of colorectal cancer (CRC) is still unknown. To investigate the effects of GPR84 on bone metastasis of CRC, the murine CRC cell line MC-38 was injected into tibial bone marrow. We found that the expression of GPR84 in BMMs was gradually downregulated during bone metastasis of CRC, and the activation of GPR84 significantly prevented osteoclastogenesis in the tumor microenvironment. Mechanistically, the MAPK pathway mediated the effects of GPR84 on osteoclast formation. Moreover, we found that IL-11 at least partly inhibited the expression of GPR84 in the tumor microenvironment through the inactivation of STAT1. Additionally, activation of GPR84 could prevent osteolysis during bone metastasis of CRC. Our results suggest that CRC cells downregulate the expression of GPR84 in BMMs to promote osteoclastogenesis in an IL-11-dependent manner. Thus, GPR84 could be a potential therapeutic target to attenuate bone destruction induced by CRC metastasis.

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“…Furthermore, circ0021205 is a non-coding circRNA that promotes cancer progression in cholangiocarcinoma and non-small cell lung cancer (NSCLC) (138). In patients with colorectal cancer (CRC), upregulated miRNA-7062-5p inhibits G protein-coupled receptor 65, thus promoting osteoclast genesis during bone metastasis (139). Long intergenic non-coding RNA (LINC)02257 is a survival-associated enhancer RNA serving important immunotherapy roles in a number of cancer types (140).…”

Section: Stromal Cellsmentioning

confidence: 99%

Role of the tumor microenvironment in cancer hallmarks and targeted therapy (Review)

et al. 2022

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Genetic alterations drive tumor onset and progression. However, the cross-talk between tumor cells and the benign components of the surrounding stroma can also promote the initiation, progression and metastasis of solid tumors. These cellular and non-cellular stromal components form the tumor microenvironment (TME), which co-evolves with tumor cells. Their dynamic and mutualistic interactions are currently considered to be among the distinctive hallmarks of cancer. Biochemical and physical cues from the TME serve an essential role in regulating tumor onset and progression. They are also associated with resistance to treatment and poor prognosis in patients with cancer. Therefore, a deep understanding of the TME is vital for developing potent anticancer therapeutics and improving patient outcomes. The present review aims to review the biology of both cellular and non-cellular constituents of the TME and novel findings regarding their contribution to core as well as emerging cancer hallmarks. The present review also describes key TME markers that are either targeted in interventional clinical trials or serve as promising potential anticancer therapies. Understanding TME components and their intercellular interactions is key toward identifying the mechanisms of progression and treatment resistance. Such understanding is of utmost significance for personalized and effective cancer therapy strategies.

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miRNA-7062-5p Promoting Bone Resorption After Bone Metastasis of Colorectal Cancer Through Inhibiting GPR65

Cited by 5 publications

References 47 publications

The Long Noncoding Transcript HNSCAT1 Activates KRT80 and Triggers Therapeutic Efficacy in Head and Neck Squamous Cell Carcinoma

The Long Noncoding Transcript HNSCAT1 Activates KRT80 and Triggers Therapeutic Efficacy in Head and Neck Squamous Cell Carcinoma

GPR84 potently inhibits osteoclastogenesis and alleviates osteolysis in bone metastasis of colorectal cancer

Role of the tumor microenvironment in cancer hallmarks and targeted therapy (Review)

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