Further study showed that overexpression of miR-148a also suppressed in vivo tumor growth, and WNT10b expression and β-catenin signaling activities in tumor tissues were suppressed by miR-148a overexpression.
RLBP1 may mediate squamous cell tumorigenesis in oral cavity, independently of the RAS protein and through Akt. miR-148a/b-3p functions as a tumor suppressor by targeting RLBP1.
HOTAIRM1 was confirmed as a tumor suppressor via sponging miR-148a and promote the expression of DLGAP1, which could be regarded as an important target for the prevention and treatment of HNT.
Therefore, the current study investigated the role of different expression levels of miR-130a-3p and miR-148a-3p on drug resistance and tumor biology in four esophageal squamous cell carcinoma cell lines.
The data from the current study indicated that miR-148a was significantly downregulated in lung adenocarcinoma tissues and cell lines, and low miR-148a expression was significantly associated with advanced Tumor, Node, Metastasis stages and lymph node metastasis, as well as the shorter survival time of patients.
The clinicopathological analysis revealed that a decrease of miR-148a was significantly correlated with lymph-node metastasis (P<0.01) and tumor node metastasis (TNM) stage (P<0.05).
In conclusion, quantitative proteomic technology revealed that miR-148a may regulate a panel of tumor-associated proteins to suppress metastasis in NSCLC.
miRNAs are involved in many physiologic and disease processes by virtue of degrading specific mRNAs or inhibiting their translation. miR-148a has been implicated in the control of tumor growth and cholesterol and triglyceride homeostasis using in vitro or in vivo gene expression- and silencing-based approaches.
<b>Results:</b> We identified 4 candidates, miR-7, miR-132, miR-335 and miR-148a, which deregulation seems to be a common event in the development of resistance to cisplatin in both tumor types. miR-7 presented specific methylation in resistant cell lines, and was associated with poorer prognosis in ovarian cancer patients.
Next to regulation mechanisms that control the expression of this miRNA family, we will focus on (i) the role of miR-148a in regulating B and T lymphocyte function and its role in associated diseases and (ii) the importance of miR-148/-152 family members for cancer initiation, tumor growth and metastasis formation.
Our findings reveal that miR-148a is an indirect tumor suppressor that modulates colitis and colitis-associated tumorigenesis by suppressing the expression of signaling by NF-κB and STAT3 and their pro-inflammatory consequences.
We have found that miR-148a exhibits properties as a tumor suppressor as its expression is inversely correlated with the ability of both human and mouse breast cancer cells to colonize the lung in mouse xenograft tumor models.