MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2

Liang, Aibin; Luo, Xiaojun; Xiong, Yan; Jiang, Shan

doi:10.1080/21655979.2021.1951930

Cited by 12 publications

(13 citation statements)

References 54 publications

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“…miR‐144 reduced the progression and migration of CRC cell by regulating GSPT1, 28 while miR‐483 contributed to the development of CRC as an oncogenic gene 29 . As a well‐known tumor suppressor, miR‐506‐3p inhibited CRC progression via EZH2 14 . Herein, we consistently confirmed that miR‐506‐3p inhibited cell proliferation and invasion during CRC progression.…”

Section: Discussionsupporting

confidence: 72%

“…10,11 MiRNAs act as tumor oncogenes or suppressors that participate in the oncogenesis of CRC. 12,13 MiR-506-3p inhibited tumorigenesis in various cancers, [14][15][16][17] and its expression in tumor tissues in patients with CRC is significantly downregulated. 14 A biological software analysis indicated the interaction between circPTK2 and miR-506-3p; however, the mechanistic insight and regulatory roles of the circPTK2/miR-506-3p in CRC progression are unclear.…”

Section: Studies Focusing On the Function Of Abnormally Expressed Cir...mentioning

confidence: 99%

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CircPTK2 accelerates tumorigenesis of colorectal cancer by upregulating AKT2 expression via miR‐506‐3p

Gong

Yang

Qiu

2022

The Kaohsiung J of Med Scie

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With the rapid increase in its incidence in the last decade, colorectal cancer (CRC) is becoming one of the most life‐threatening cancers. Circular RNA PTK2 (circPTK2) has multiple functions in oncogenesis, including in CRC. However, it remains elusive if circPTK2 also plays an important role in CRC malignancy. The levels of circPTK2, miR‐506‐3p, and AKT serine/threonine kinase 2 (AKT2) were measured by qPCR. The protein level of AKT2 was evaluated by western blotting assay. The proliferation, migration, and invasion of CRC cancer cells were evaluated by MTT, colony formation, wound‐healing, and transwell assays. The interaction between circPTK2 and miR‐506‐3p and between miR‐506‐3p and AKT2 mRNA were verified by dual‐luciferase reporter assay. The expressions of circPTK2 and AKT2 were elevated in CRC cells, with a concomitant reduction of miR‐506‐3p. The knockdown of circPTK2 suppressed the proliferation, migration, and invasion of CRC cells. CircPTK2 targeted miR‐506‐3p and negatively regulated its expression. Furthermore, miR‐506‐3p overexpression suppressed the CRC progression by downregulating the AKT2 expression. AKT2 overexpression or miR‐506‐3p inhibition restored the suppression of growth and invasiveness of CRC cancer cells caused by circPTK2 silencing. The circPTK2/miR‐506‐3p/AKT2 axis plays a novel and essential role in promoting CRC progression, providing potential targets for CRC therapeutic modality.

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Section: Discussionsupporting

confidence: 72%

Section: Studies Focusing On the Function Of Abnormally Expressed Cir...mentioning

confidence: 99%

CircPTK2 accelerates tumorigenesis of colorectal cancer by upregulating AKT2 expression via miR‐506‐3p

Gong

Yang

Qiu

2022

The Kaohsiung J of Med Scie

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“…Colorectal cancer (CRC) is a widespread human cancer and the incidence in China accounted for 10% of all diagnosed cancer cases in 2009 [ 1 ]. The diet and habits are the main factors of CRC, which leads to the increasing incidence of CRC in Asia and Africa [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of DEAD-box helicase 21 (DDX21) inhibits proliferation, cell cycle, and tumor growth in colorectal cancer via targeting cell division cycle 5-like (CDC5L)

Wang

Peng

et al. 2021

Bioengineered

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Identification of novel anti-tumor target is crucial for cancer diagnosis, prognosis, and therapeutic strategy. The study aimed to explore the roles and interaction of DEAD-box helicase 21 (DDX21) and cell division cycle 5-like (CDC5L) in colorectal cancer (CRC) progression. Levels of DDX21 and CDC5L were detected in colorectal cancer cell lines by RT-qPCR and Western blot assay. The role of DDX21 and CDC5L on the cell proliferation, cell cycle and tumor growth were evaluated both in vitro and in vivo . The interaction of DDX21 and CDC5L was predicted by The STRING publicly available data and verified by immunoprecipitation. The results showed that DDX21 was dramatically upregulated in colorectal cancer cells. In vivo and in vitro experiments revealed that downregulation of DDX21 suppressed colorectal cancer cell proliferation, colony formation, cell cycle development, and tumor growth, while overexpression of CDC5L reversed the suppressive effects of DDX21 silencing. Furthermore, DDX21 interacted with CDC5L to exert the tumor-promoting effects in CRC. In summary, the data indicate a novel role for DDX21/CDC5L in the development of CRC, which enrich the therapeutic strategy for CRC.

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“…MiRNAs are multifunctional regulators of tumorigenesis and cancer progression, and miRNAs with tumor suppressor activities have been proposed as adjuvant therapies. These miRNAs, such as miRNA-506-3p, miRNA-143, miRNA-330, miR-141-3p, and miRNA-877 [ 19–23 ], inhibit tumorigenesis or progression by targeting oncogenic genes or signaling pathways. Both in vitro and in vivo experiments by Tian et al reported the inhibition of migration and invasion by miR-130a-3p in esophageal squamous cell carcinoma cell line EC-1 [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-130a-3p suppresses colorectal cancer growth by targeting Wnt Family Member 1 (WNT1)

et al. 2021

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The microRNA miR-130a-3p (miR-130a-3p) has anti-tumor activity against numerous cancer types. Further, miR-130a-3p may target Wnt signaling, which is a critical pathway regulating tumorigenesis. Functions of miR-130a-3p in colorectal cancer (CRC) and contributions of Wnt1 pathway modulation, however, have not been examined, hence the exploration on these two aspects. In this study, in comparison with normal controls, both CRC tissue and multiple CRC cell lines showed downregulated miR-130a-3p. MiR-130a-3p overexpression contributed to a decrease in CRC cell proliferation. Additionally, its overexpression also caused reduced expression of WNT Family Member 1 (WNT1) and downstream WNT pathway factors c-myc and cyclin D1. Dualluciferase assay revealed WNT1 as a direct target of miR-130a-3p, and further the inhibitory effect of miR-130a-3p on c-myc and cyclin D1 was proved to be reversed by overexpressed WNT1. Collectively, miR-130a-3p inhibits CRC growth by directly targeting WNT1, and miR-130a-3p and WNT1 pathway-associated factors are defined as potential targets for CRC treatment.

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MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2

Cited by 12 publications

References 54 publications

CircPTK2 accelerates tumorigenesis of colorectal cancer by upregulating AKT2 expression via miR‐506‐3p

CircPTK2 accelerates tumorigenesis of colorectal cancer by upregulating AKT2 expression via miR‐506‐3p

Downregulation of DEAD-box helicase 21 (DDX21) inhibits proliferation, cell cycle, and tumor growth in colorectal cancer via targeting cell division cycle 5-like (CDC5L)

MiR-130a-3p suppresses colorectal cancer growth by targeting Wnt Family Member 1 (WNT1)

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