<scp>miR</scp>‐29a‐3p promotes migration and invasion in ameloblastoma via Wnt/β‐catenin signaling by targeting catenin beta interacting protein 1

Liu, Sai; Liu, Dongjuan; Liu, Jinwen; Zhong, Ming

doi:10.1002/hed.26888

Cited by 11 publications

(10 citation statements)

References 56 publications

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“…The RAF1-MEK/ERK-ARL4C axis may function in cooperation with the BRAFV600E-MEK/ERK pathway to promote ameloblastoma development [50]. The microRNA miR-29a-3p promotes migration and invasion in ameloblastoma via Wnt/β-catenin signaling by targeting catenin beta interacting protein 1 [51]. The upfront treatment with BRAF inhibitors resulting in substantial tumor regression has enabled non-mutilating complete surgical removal, ad integrum bone regeneration, and organ preservation.…”

Section: Recent Advancesmentioning

confidence: 99%

Ameloblastoma: An Updated Narrative Review of an Enigmatic Tumor

Ghai¹

2022

Cureus

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Ameloblastoma is one of the most common benign odontogenic tumors of the jaw that constitutes about 10% of all tumors that arise in the mandible and maxilla. It is a slow-growing but locally invasive tumor that presents with painless swelling of the mandible or maxilla. The World Health Organization (WHO) classification of 2017 describes ameloblastomas of the following four types: ameloblastoma; unicystic ameloblastoma; extraosseous/peripheral ameloblastoma; and metastasizing ameloblastoma. The diagnosis of ameloblastoma requires computerized tomography (CT) imaging as well as a biopsy. A biopsy is helpful in differentiating ameloblastoma from ossifying fibroma, osteomyelitis, giant cell tumor, cystic fibrous dysplasia, myeloma, and sarcoma. The best treatment of ameloblastoma is aggressive en bloc resection with simultaneous reconstruction. The high recurrence rate and large tissue defects have been long-standing issues in the treatment of ameloblastoma. Recent molecular developments strongly suggest the possibility of targeted therapy with better outcomes in ameloblastomas. We present a detailed updated narrative review of our current understanding and management of this enigmatic tumor.

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Section: Recent Advancesmentioning

confidence: 99%

Ameloblastoma: An Updated Narrative Review of an Enigmatic Tumor

Ghai¹

2022

Cureus

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“…miR-29a-3p directly targets the Wnt/β-catenin signaling pathway in several types of cancer including ameloblastoma ( 39 ) and gastric cancer ( 8 ). To further investigate the underlying mechanisms involved, the association between miR-29a-3p and Wnt/β-catenin signaling pathway in NSCLC was further examined next.…”

Section: Discussionmentioning

confidence: 99%

“…miRNAs could stimulate early-stage NSCLC progression by simultaneously stimulating Wnt/β-catenin signaling ( 6 ). Moreover, it has been reported that miR-29a-3p regulates the migration and invasion in ameloblastoma via the Wnt/β-catenin pathway ( 39 ). The Wnt/β-catenin pathway was inactivated in a miR-29a-3p-dependent manner in GC cells ( 8 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑29a‑3p inhibits the malignant characteristics of non‑small cell lung cancer cells by reducing the activity of the Wnt/β‑catenin signaling pathway

Zhang

Han

et al. 2022

Oncol Lett

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MicroRNAs (miRNAs) can influence non-small cell lung cancer (NSCLC) in a tumor-suppressive and oncogenic manner. The present study aimed to investigate the effects and underlying mechanisms of miR-29a-3p in NSCLC. NSCLC cell lines (A549, H1299, and H460) and a normal lung epithelial cell line (BEAS-2B) were used. Additionally, a mouse lung tumor xenograft model was established using A549 cells and used to determine the effects of miR-29a-3p on NSCLC in vivo. Tumor volumes were measured every week. The expression of miR-29a-3p in cells and lung tissues were detected by RT-qPCR. Cell proliferation was detected using Cell Counting Kit-8 and EdU assays. Migration and invasion were assessed using wound healing and Transwell invasion assays, respectively. Ki-67 expression was detected using immunohistochemical staining. The expression levels of Wnt3a and β-catenin were determined using western blotting. miR-29a-3p expression was significantly downregulated in NSCLC cells and mice. In contrast to miR-29a-3p knockdown, miR-29a-3p overexpression decreased NSCLC cell proliferation, migration, and invasion as well as tumor growth in in the NSCLC mouse model. Moreover, miR-29a-3p overexpression decreased the protein expression levels of Wnt3a and β-catenin. The inhibitory effects of miR-29a-3p on NSCLC cells were reversed by LiCl (an activator of the Wnt signaling pathway). In conclusion, miR-29a-3p prevented NSCLC tumor growth and cell proliferation, migration, and invasion by inhibiting the Wnt/β-catenin signaling pathway. This finding offers novel insights into the prognosis and treatment of NSCLC.

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“…Liu et al found that miR-29a-3p levels in tissues were higher than normal in ameloblastoma. Additional research showed that miR-29a-3p directly targets the β-catenin interacting protein 1 (CTNNBIP1), which negatively regulated the activity of the Wnt/-βcatenin pathway and facilitates cell migration and invasion [ 72 ]. Sikder et al discovered PC4, a transcriptional coactivator, as a target of miR-29a-3p in breast cancer, which led to tumor growth both in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 99%

MiR-29a-3p: a potential biomarker and therapeutic target in colorectal cancer

Cao

2022

Clin Transl Oncol

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Cancer is frequently caused by microRNAs, which control post-transcriptional levels of gene expression by binding to target mRNAs. MiR-29a-3p has recently been shown to play a twofold function in the majority of malignancies, including colorectal cancer (CRC), according to mounting evidence. Here, we not only briefly summarize such connection between miR-29a-3p and cancers, but aslo primarily evaluate the miR-29a-3p expression pattern, clinical applicability, and molecular mechanisms in CRC to provide a guide for future studies. This review established the diagnostic and prognostic value of miR-29a-3p abnormalty in a variety of clinical samples for CRC. Furthermore, current molecular mechanisms of miR-29a-3p for regulating cancerous biological processes such growth, invasion, metastasis, the epithelial-mesenchymal transformation process, and immunomodulation through its upstream regulatory factors and downstream targeted genes were briefly explored. More specifically, miR-29a-3p has been linked to a few medications that have been shown to have anticancer benefits. To sum up, miR-29a-3p is a promising biomarker and prospective therapeutic target for the diagnosis and prognosis of CRC, but further research is still needed to establish a theoretical basis for more practical applications.

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miR‐29a‐3p promotes migration and invasion in ameloblastoma via Wnt/β‐catenin signaling by targeting catenin beta interacting protein 1

Cited by 11 publications

References 56 publications

Ameloblastoma: An Updated Narrative Review of an Enigmatic Tumor

Ameloblastoma: An Updated Narrative Review of an Enigmatic Tumor

miR‑29a‑3p inhibits the malignant characteristics of non‑small cell lung cancer cells by reducing the activity of the Wnt/β‑catenin signaling pathway

MiR-29a-3p: a potential biomarker and therapeutic target in colorectal cancer

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