The Novel Target of Colorectal Carcinoma: TRIM44 Regulates Cell Migration and Invasion via Activation of CXCR4/NF-κB Signaling.

Tripartite motif containing 44 (TRIM44) has been reported to regulate various biological effects in malignant cancers and matrix Metalloproteinases has been demonstrated to be associated with cancer cell migration and invasion. Nonetheless, the expression and molecular mechanism of TRIM44 in colorectal cancer (CRC) remain rarely known. TRIM44 was overexpressed or knocked down in CRC cells. Subsequently, the effects of TRIM44 on cell migration and invasion as well as underlying molecular mechanisms were detected. Data showed that TRIM44 was highly expressed in CRC cell lines. Downregulation of TRIM44 inhibited the cell viability, migration, and invasion in SW-480 cells. In addition, overexpression of TRIM44 enhanced the expression of NF-κB and CXCR4, and enhanced the binding between NF-κB and CXCR4 promoter region. In summarize, TRIM44 may serve as a potential target for CRC diagnosis and progression.

A rare and rapidly progressing renal chondrosarcoma: a case report.

Mesenchymal chondrosarcoma of the kidney is a rare soft tissue sarcoma. We report a 64-year-old female with a right renal pelvic mass. After a right nephrectomy was performed, the histopathological examination confirmed the diagnosis to be primary extraskeletal mesenchymal chondrosarcoma. After the surgical removal of the tumor, the patient suffered rapid disease progression.

HPT axis­independent TSHß splice variant regulates the synthesis of thyroid hormone in mice.

Thyroid stimulating hormone (TSH) consists of an α­subunit and a unique ß­subunit. The first in­frame TSHß splice variant produced by the cells of immune system was identified in 2009. The TSHß splice variant and native TSHß exhibit different expression profiles, and research has been conducted to elucidate the role of the TSHß splice variant in different diseases. However, understanding of the fundamental physiological characteristics of the TSHß splice variant is currently limited. To verify whether the TSHß splice variant has the potential to induce thyroid follicular cells to synthesize thyroid hormone, in vivo and in vitro stimulation experiments were conducted in the present study. A total of 60 C57BL/6 mice were divided into control­, 5 and 10 µg TSHß splice variant­treated groups at random. Mice were sacrificed at 0.5, 1 and 4 h after intraperitoneal injection, and serum levels of tri­iodothyronine (T3) and thyroxine (T4) were determined using a radioimmunoassay. Thyroid follicular cells were isolated from the thyroids of mice, and stimulated with 2 µg/ml TSHß splice variant. Supernatants were collected, and the levels of T3 and T4 were detected. The protein expression levels of the sodium­iodide symporter, thyroperoxidase and thyroglobulin in thyroid follicular cells were quantified using western blot analysis. To verify whether the TSHß splice variant expression was regulated by the hypothalamus­pituitary­thyroid (HPT) axis, similar to native TSHß, a total of 60 C57BL/6 mice were equally divided into control, 2 mg/kg T3 intraperitoneal injection and 0.05 mg/kg thyroid­releasing hormone intraperitoneal injection groups at random. Mice were sacrificed at 1 and 4 h after injection. Alterations in the expression of the TSHß splice variant in the pituitary, thyroid, peripheral blood leukocytes and spleen tissues were detected using western blot analysis. The present study demonstrated that the TSHß splice variant is not regulated by the HPT axis and may affect thyroid hormone synthesis. Modifications in the expression of the TSHß splice variant may occur in a uniquely regulated manner to provide peripheral immunological compartments with a source of activated cells, particularly under immune stress.