SPTBN1 inhibits growth and epithelial-mesenchymal transition in breast cancer by downregulating miR-21

Wu, Huihui; Chen, Shuyi; Liu, Chenyang; Li, Jiajia; Wei, Xiangxiang; Jia, Minghan; Guo, Jr-Hung; Jin, Jiayu; Meng, Dan; Zhi, Xiuling

doi:10.1016/j.ejphar.2021.174401

Cited by 13 publications

(12 citation statements)

References 45 publications

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“…It was verified that SPTBN1 could be a novel therapeutic target for osteoporosis because SPTBN1 could facilitate the proliferative and differentiative capabilities of osteoblasts 10 . Additionally, the depletion of SPTBN1 exhibited promotive effects on the migrative ability of triple‐negative breast cancer (TNBC), implying that SPTBN1 was a critical regulator in TNBC advancement 19 . Moreover, the loss of SPTBN1 could contribute to the changes in cell apoptosis 20 .…”

Section: Discussionmentioning

confidence: 97%

“… 10 Additionally, the depletion of SPTBN1 exhibited promotive effects on the migrative ability of triple‐negative breast cancer (TNBC), implying that SPTBN1 was a critical regulator in TNBC advancement. 19 Moreover, the loss of SPTBN1 could contribute to the changes in cell apoptosis. 20 In this paper, it was discovered that the mRNA and protein levels of SPTBN1 were greatly descended in RA‐FLSs.…”

Section: Discussionmentioning

confidence: 99%

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SPTBN1 attenuates rheumatoid arthritis synovial cell proliferation, invasion, migration and inflammatory response by binding to PIK3R2

Dai¹,

Xu²,

Yang³

et al. 2022

Immunity Inflam & Disease

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Background As an autoimmune systemic disorder, rheumatoid arthritis (RA) features chronic inflammation as well as synovial infiltration of immune cells. This study was designed with the purpose of discussing the hidden mechanism of SPTBN1 and exploring favorable molecular‐targeted therapies. Methods With the application of RT‐qPCR and western blot, the expressions of SPTBN1 and PIK3R2 before or after transfection were estimated. Besides, Cell Counting Kit‐8, Edu, wound healing, transwell, enzyme‐linked immunosorbent assay, and TUNEL were adopted for the evaluation of the viability, proliferation, migration, invasion, inflammatory response, and apoptosis of fibroblast‐like synoviocyte (FLS). In addition, the interaction of SPTBN1 and PIK3R2 was testified by applying immunoprecipitation (IP) and western blot was utilized for the assessment of migration‐, apoptosis‐, and PI3K/AKT signal‐related proteins. Results It was discovered that SPTBN1 declined in RA synovial cells and its overexpression repressed the proliferation, migration, invasion, and inflammation of RA‐FLSs but promoted apoptosis. IP confirmed that SPTBN1 could bind to PIK3R2 in FLSs. To further figure out the hidden mechanism of SPTBN1 in RA, a series of functional experiments were carried out and the results demonstrated that the reduced expressions of MMP2, MMP9, IL‐8, IL‐1β, IL‐6, and Bcl2 as well as increased levels of Bax and cleaved caspase3 in SPTBN1‐overexpressed RA‐FLSs were reversed by PIK3R2 depletion, revealing that SPTBN1 repressed the migration and inflammation and promoted the apoptosis of RA‐FLSs via binding to PIK3R2. Results obtained from western blot also revealed that PIK3R2 interference ascended the contents of p‐PI3K and p‐AKT in SPTBN1‐overexpressed RA‐FLSs, implying that SPTBN1 repressed PI3K/AKT signal in RA via PIK3R2. Discussion SPTBN1 alleviated the proliferation, migration, invasion, and inflammation in RA via interacting with PIK3R2.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

SPTBN1 attenuates rheumatoid arthritis synovial cell proliferation, invasion, migration and inflammatory response by binding to PIK3R2

Dai¹,

Xu²,

Yang³

et al. 2022

Immunity Inflam & Disease

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“…The loss of SPTBN1 activates Wnt signalling and promotes the acquisition of the stemness feature in tumour cells, ultimately leading to the progression of malignant tumours 54 . Reviewing the literature, we found that SPTBN1 was downregulated in breast cancer cells and was a key regulator that inhibits EMT and breast cancer growth 55 . This study found that YTHDF1 promotes EMT and breast cancer progression in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Prognostic implications of N6-methyladenosine RNA regulators in breast cancer

Tai

Wang

Guo

et al. 2022

Sci Rep

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The significance of N6-methyladenosine (m6A) RNA modifications in the progression of breast cancer (BC) has been recognised. However, their potential role and mechanism of action in the tumour microenvironment (TME) and immune response has not been demonstrated. Thus, the role of m6A regulators and their downstream target gene components in BC remain to be explored. In this study, we used a series of bioinformatics methods and experiments to conduct exploratory research on the possible role of m6A regulators in BC. First, two regulatory modes of immune activation and inactivation were determined by tumour classification. The TME, immune cell infiltration, and gene set variation analysis results confirmed the reliability of this pattern. The prognostic model of the m6A regulator was established by the least absolute shrinkage and selection operator and univariate and multivariate Cox analyses, with the two regulators most closely related to survival verified by real-time quantitative reverse transcription polymerase chain reaction. Next, the prognostic m6A regulator identified in the model was crossed with the differential copy number of variant genes in invasive BC (IBC), and it was determined that YTHDF1 was a hub regulator. Subsequently, single-cell analysis revealed the expression patterns of m6A regulators in different IBC cell populations and found that YTHDF1 had significantly higher expression in immune-related IBC cells. Therefore, we selected the intersection of the BC differential expression gene set and the differential expression gene set of a cell line with knocked-down YTHDF1 in literature to identify downstream target genes of YTHDF1, in which we found IFI6, EIR, and SPTBN1. A polymerase chain reaction was conducted to verify the results. Finally, we confirmed the role of YTHDF1 as a potential prognostic biomarker through pan-cancer analysis. Furthermore, our findings revealed that YTHDF1 can serve as a new molecular marker for BC immunotherapy.

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“…In the therapy of breast cancer, various miRNAs play significant roles, including the following: MiR-21: this is one of the most commonly identified miRNAs associated with breast cancer. MiR-21 has been shown to contribute to breast cancer development and progression by regulating a range of genes responsible for proliferation, angiogenesis, and invasion of cancer cells [ 170 , 171 , 172 , 173 , 174 ]. MiR-34a: miR-34a has been shown to inhibit proliferation and induce apoptosis of breast cancer cells, making it a potential therapeutic target [ 175 , 176 , 177 ].…”

Section: The Role Of Mirnasmentioning

confidence: 99%

“…MiR-21: this is one of the most commonly identified miRNAs associated with breast cancer. MiR-21 has been shown to contribute to breast cancer development and progression by regulating a range of genes responsible for proliferation, angiogenesis, and invasion of cancer cells [ 170 , 171 , 172 , 173 , 174 ].…”

Section: The Role Of Mirnasmentioning

confidence: 99%

Harnessing Epigenetics for Breast Cancer Therapy: The Role of DNA Methylation, Histone Modifications, and MicroRNA

Szczepanek

Skorupa

Jarkiewicz‐Tretyn³

et al. 2023

IJMS

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Breast cancer exhibits various epigenetic abnormalities that regulate gene expression and contribute to tumor characteristics. Epigenetic alterations play a significant role in cancer development and progression, and epigenetic-targeting drugs such as DNA methyltransferase inhibitors, histone-modifying enzymes, and mRNA regulators (such as miRNA mimics and antagomiRs) can reverse these alterations. Therefore, these epigenetic-targeting drugs are promising candidates for cancer treatment. However, there is currently no effective epi-drug monotherapy for breast cancer. Combining epigenetic drugs with conventional therapies has yielded positive outcomes and may be a promising strategy for breast cancer therapy. DNA methyltransferase inhibitors, such as azacitidine, and histone deacetylase inhibitors, such as vorinostat, have been used in combination with chemotherapy to treat breast cancer. miRNA regulators, such as miRNA mimics and antagomiRs, can alter the expression of specific genes involved in cancer development. miRNA mimics, such as miR-34, have been used to inhibit tumor growth, while antagomiRs, such as anti-miR-10b, have been used to inhibit metastasis. The development of epi-drugs that target specific epigenetic changes may lead to more effective monotherapy options in the future.

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SPTBN1 inhibits growth and epithelial-mesenchymal transition in breast cancer by downregulating miR-21

Cited by 13 publications

References 45 publications

SPTBN1 attenuates rheumatoid arthritis synovial cell proliferation, invasion, migration and inflammatory response by binding to PIK3R2

SPTBN1 attenuates rheumatoid arthritis synovial cell proliferation, invasion, migration and inflammatory response by binding to PIK3R2

Prognostic implications of N6-methyladenosine RNA regulators in breast cancer

Harnessing Epigenetics for Breast Cancer Therapy: The Role of DNA Methylation, Histone Modifications, and MicroRNA

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