The expression of miR-370 was decreased by CXCL12 treatment in NFPAs. miR-370-3p was predicted and verified to target HMGA2 as a tumor suppressor gene.
The xenograft tumor model was performed to examine the influence of the lncRNA FOXD2-AS1/miR-185-5p/HMGA2 network on the biological functions of glioma cells.
Our results reveal that HMGA1 and HMGA2 mRNA and protein are overexpressed in ECC, but only <i>HMGA1</i> expression is associated with increased histological grade and tumor size.
In vivo, transfection with miR-9 mimics down-regulated the expression of HMGA2, thus leading to a dramatic reduction in tumor growth in a mouse xenograft model.
Thick-walled vessels in HLM were composed of mostly HMGA2-positive tumor cells, and HLM with HMGA2 overexpression also showed CD34-positive tumor vessel-supporting pericytes.
Finally, there was a significant negative correlation between the expression levels of HMGA2 and miR‑363‑3p in liver cancer tissues. miR‑363‑3p was identified as an important tumor suppressor in liver cancer via targeting HMGA2, which may have potential benefits in liver cancer therapy.
In carcinomas, overexpression of high-mobility-group A2 (HMGA2) in cancer cells would lead to tumor development and epithelial to mesenchymal transition (EMT), promoting metastasis.
Furthermore, we reveal that HMGA2-mediated EMT is closely linked with the expression of POSTN that inhibits EMT, as a tumor suppressor, by gene profiling analyses.
HMGA2 overexpression in ULM is not only related to tumor development but also plays a role in controlling cellular proliferation through the AKT pathway.
Furthermore, high-mobility group AT-hook 2 expression in the fibro-adipocytes of this tumor indicated that these cells are an integral component of the pancreatic lipomatous hamartoma.
Immunohistochemical staining of prostate tissue microarray revealed low membrane expression in normal epithelial prostate cells, and that expression increased with tumor grade as well as a switch from predominantly cytoplasmic HMGA2 in lower tumor grades, to mostly nuclear in high grade and bone metastatic tissue.
Further, in BABL/c nude mice, CD8<sup>+</sup> T cells depleting mice and NK cells depleting nude mice, the promotion of tumor growth was significantly diminished, suggesting that both NK cells and CD8<sup>+</sup> T cells were involved in the tumor promoting process mediated by intrinsic TIGIT.
Normal and tumor tissue obtained from premenopausal women who underwent hysterectomy were collected after surgery and DNA, RNA and proteins were isolated and analyzed for MED12 mutations using Sanger sequencing, HMGA2 mRNA expression by quantitative PCR and HMGA2 protein detection by western blot and immunohistochemistry.
The aim of the study was to investigate the immunohistochemical expression profiles of MMP-9, PTTG, HMGA2, and Ki-67 in recurrent and nonrecurrent ACTH-secreting pituitary tumors and to identify their associations with tumor behavior and recurrence status.