MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

Li, Qunying; Ren, Pingping; Shi, Pengfei; Chen, Yihan; Xiang, Feixiang; Zhang, Li; Wang, Jing; Lv, Qing; Xie, Mingxing

doi:10.1097/cad.0000000000000498

Cited by 26 publications

(24 citation statements)

References 36 publications

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“… 8 For example, miR-198 inhibited cell proliferation and migration and promoted cell adhesion in aggressive breast cancer by targeting CUB domain-containing protein 1 (CDCP1); 9 miR-340 suppressed the migration, invasion, and metastasis of breast cancer cells through modulating Wnt/β-catenin signaling pathway; 10 miR-148a accelerated cell apoptosis and restricted growth of breast cancer cells via regulating B-cell lymphoma 2 (Bcl-2). 11 Therefore, miRNAs are regarded as reliable prognostic markers, promising therapeutic targets, or new drugs, which would be essential in the prevention and treatment of breast cancer. 12 …”

Section: Introductionmentioning

confidence: 99%

Targeting of GIT1 by miR-149* in breast cancer suppresses cell proliferation and metastasis in vitro and tumor growth in vivo

Dong¹,

Cheng²,

Liu³

et al. 2017

OTT

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Breast cancer remains a major cause of cancer-related death in women worldwide. Dysregulation of microRNAs (miRNAs) is involved in the initiation and progression of breast cancer. Moreover, it was found that GIT1 was widely involved in the development of many human cancers. Herein, we aimed to investigate the expression changes of miR-149* and GIT1 and the functional effects of miR-149*/GIT1 link in breast cancer. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot (WB) were used to examine the expression levels of miR-149* and GIT1. Dual luciferase reporter assay was utilized to confirm the target interaction between miR-149* and GIT1. The biological functions, including cell proliferation, invasion, and migration, of miR-149* and GIT1 were determined by MTT assay and Transwell assays, respectively. Eventually, the tumor xenograft model in nude mice injected with stable transfected MDA-MB-231 cells was established to verify the effects of miR-149* and GIT1 on tumor growth. Our results showed that miR-149* expression was decreased, whereas GIT1 expression was increased in clinical samples of breast cancer. Based on the inverse expression trend between miR-149* and GIT1, we further demonstrated that miR-149* indeed directly targets GIT1. Subsequently, it was observed that inhibition of miR-149* significantly promoted cell proliferation, invasion, and migration, but the ability of cell proliferation, invasion, and migration was obviously declined after silencing of GIT1 in MDA-MB-231 cells transfected with miR-149* mimic and/or si-GIT1. Finally, it was also found that elevated miR-149* decelerated the tumor growth, while restored GIT1 accelerated the tumor growth in nude mice after 35 days of tumor xenograft. Collectively, these findings concluded that miR-149* might exert a tumor suppressive role in breast cancer by targeting GIT1.

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Section: Introductionmentioning

confidence: 99%

Targeting of GIT1 by miR-149* in breast cancer suppresses cell proliferation and metastasis in vitro and tumor growth in vivo

Dong¹,

Cheng²,

Liu³

et al. 2017

OTT

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“…It has been shown that miR-148a regulates ERα expression through DNMT1-mediated DNA methylation in BC cells [366]. In contrast, it has been reported that miR-148a targets B-cell lymphoma 2 (BCL-2), which is frequently upregulated in BC [367]. Nuclear receptor NR4A1 (Nur77) promotes BC invasion and metastasis by activating TGF-β signaling [368,369].…”

Section: Breast Cancermentioning

confidence: 99%

Exosomes of pasteurized milk: potential pathogens of Western diseases

Melnik

Schmitz

2019

J Transl Med

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Milk consumption is a hallmark of western diet. According to common believes, milk consumption has beneficial effects for human health. Pasteurization of cow's milk protects thermolabile vitamins and other organic compounds including bioactive and bioavailable exosomes and extracellular vesicles in the range of 40-120 nm, which are pivotal mediators of cell communication via systemic transfer of specific micro-ribonucleic acids, mRNAs and regulatory proteins such as transforming growth factor-β. There is compelling evidence that human and bovine milk exosomes play a crucial role for adequate metabolic and immunological programming of the newborn infant at the beginning of extrauterine life. Milk exosomes assist in executing an anabolic, growth-promoting and immunological program confined to the postnatal period in all mammals. However, epidemiological and translational evidence presented in this review indicates that continuous exposure of humans to exosomes of pasteurized milk may confer a substantial risk for the development of chronic diseases of civilization including obesity, type 2 diabetes mellitus, osteoporosis, common cancers (prostate, breast, liver, B-cells) as well as Parkinson's disease. Exosomes of pasteurized milk may represent new pathogens that should not reach the human food chain.

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“…Furthermore, increasing miRNAs has been reported to play an important role in colorectal cancer, such as miR-144, miR-495, miR-590, miR-6803 (8–11). miR-148a has been reported to be downregulated in many kinds of tumors including breast cancer, renal cell carcinoma and endometrial cancer (12–14). According to Li et al (12), miR-148a promotes apoptosis and inhibits growth of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

miR‑148a inhibits cell proliferation and migration through targeting ErbB3 in colorectal cancer

et al. 2019

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Colorectal cancer is a common gastrointestinal cancer ranking in third place of all cancers. Downregulation of miR-148a has been observed in many tumors, and miR-148a was found to be an oncogene in colorectal cancer. The aim of our study was to investigate the molecular mechanisms by which miR-148a and ErbB3 proliferate and migrate in colorectal cancer. The expression of miR-148a and ErbB3 were measured by western blot analysis and RT-qPCR. MTT and transwell assays were performed to analyze the proliferative and migratory abilities. The dual luciferase reporter assay was employed to confirm miR-148a regulated the expression of ErbB3 in colorectal cancer. It was discovered that miR-148a was overexpressed while ErbB3 expression was low in colorectal cancer, and the mRNA level of miR-148a had a negative correlation with the expression of ErbB3. Upregulation of miR-148a suppressed the proliferation and migration in colorectal cancer cells. Furthermore, ErbB3 was identified as a direct target of miR-148a, which suppressed the proliferation and migration through directly binding to the 3′UTR of ErbB3 mRNA. This study established that miR-148a inhibited the proliferative and migratory abilities through mediating the expression of ErbB3. The newly identified miR-148a/ErbB3 axis provides novel insight into the pathogenesis of colorectal cancer, and represents a potential target for treatment of colorectal cancer.

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MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

Cited by 26 publications

References 36 publications

Targeting of GIT1 by miR-149* in breast cancer suppresses cell proliferation and metastasis in vitro and tumor growth in vivo

Targeting of GIT1 by miR-149* in breast cancer suppresses cell proliferation and metastasis in vitro and tumor growth in vivo

Exosomes of pasteurized milk: potential pathogens of Western diseases

miR‑148a inhibits cell proliferation and migration through targeting ErbB3 in colorectal cancer

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