Activity

Tissue-specific 5-hydroxymethylcytosine landscape from the man genome.

Mechanistically, LINC00525 acted as a molecular sponge of microRNA-505-3p (miR-505-3p) and upregulated the expression of high mobility group box 1 (HMGB1), which is directly targeted by miR-505-3p. Rescue assays indicated that increasing the output of miR-505-3p-HMGB1 axis attenuated the effects of LINC00525 depletion on chordoma cells.

LINC00525, a pro-oncogenic long noncoding RNA, promotes chordoma progression by regulating the miR-505-3p-HMGB1 axis. The LINC00525-miR-505-3p-HMGB1 pathway may be a novel therapeutic target in chordoma.

LINC00525, a pro-oncogenic long noncoding RNA, promotes chordoma progression by regulating the miR-505-3p-HMGB1 axis. The LINC00525-miR-505-3p-HMGB1 pathway may be a novel therapeutic target in chordoma.

Caspase recruitment domain-containing protein 9 (CARD9) is expressed at high levels in bone marrow cells and has a crucial role in innate immunity. Current studies indicate that CARD9 also plays a key role in tumor progression, but there are few reports on the role of CARD9 in lung cancer. The aim of this study was to clarify the role of CARD9 in lung adenocarcinoma.

Lung adenocarcinoma tumor samples from 74 patients who underwent complete resection at Kobe University Hospital from January 2014 to December 2014 were analyzed by immunohistochemistry. The role of CARD9 in cancer cells was analyzed using lung cancer cell lines treated with CARD9 siRNA.

High expression of CARD9 was observed in 32.4% of tumors, and compared to low expression of CARD9, high expression was associated with poorer overall survival (P = 0.0365). Univariate and multivariate analyses showed that high expression of CARD9 was an independent prognostic factor. Knockdown of CARD9 in lung adenocarcinoma cells inhibited proliferation but did not increase apoptosis. In addition, CARD9 activated the NF-κB pathway in a lung adenocarcinoma cell line.

CARD9 was shown to be an independent prognostic factor of poor outcome for lung cancer and may represent a molecular target for treatment.

CARD9 was shown to be an independent prognostic factor of poor outcome for lung cancer and may represent a molecular target for treatment.

Sanguinarine (SNG) is a benzophenanthridine alkaloid obtained from the roots of

and has an anticancer effect. The aim of this study was to explore the mechanism of SNG in inhibiting macrophages via regulating the exosomes derived from lung carcinoma cells to reduce metastasis and proliferation of lung carcinoma.

Human lung cancer cells (A549 cells) were treated with 4μM of SNG. Exosomes of A549 cells were extracted from A549 cells supernatant, and THP-1 cells were cultured with exosomes. Then, the supernatant of THP-1 cells was collected and cultured with A549 cells. Cell proliferation was measured via plate clone formation and CCK-8 assays. Migration was assessed by using Transwell assay and scratch test. see more see more Cellular invasion was detected by Transwell assay. Apoptosis was determined using flow cytometry. Moreover, the protein expressions of GAPDH, P65 and P-P65 in THP-1 cells were measured by Western blot. Levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and chemotactic cytokines ligand 2 proliferation, and migration of A549 cells were inhibited, and the apoptosis was promoted. The mechanism is possibly associated with the inhibition of NF-κB pathway in THP-1 cells.

Theabrownin (TB), a main pigment and bioactive component of tea, has been shown anti-tumor activities against carcinomas, but its effects on hepatocellular carcinoma (HCC) remain unclear.

Hepatocellular carcinoma Huh7 cells were used for analyses. Cell viability assay was performed to determine TB’s anti-proliferative effect, and flow cytometry with annexin V-FITC/PI double staining and DAPI staining were performed to determine its pro-apoptotic effect. Real-time PCR and Western blot assays were conducted to detect the molecular actions of TB. And a xenograft model of zebrafishes was established to evaluate the in vivo effect of TB. SP600125 (JNK inhibitor) was in vivo and in vitro used to verify the regulatory role of the JNK signaling pathway in the anti-hepatic carcinoma mechanism of TB.

TB exerted significant anti-proliferative and pro-apoptotic effects on Huh7 cells in a dose-dependent manner. The molecular data showed that TB up-regulated the gene expressions of

and

and up-regulated the protein expressions of ASK-1, Bax, phosphorylated JNK, and phosphorylated c-Jun with down-regulation of Bcl-2. The in vivo data showed that TB exerted significant tumor-inhibitory effect which was even stronger than that of cis-platinum. Furthermore, the JNK inhibitor significantly weakened TB’s effects both in vivo and in vitro and blocked the related molecular pathway.

TB exerts anti-proliferative, pro-apoptotic, and tumor-inhibitory effects on Huh7 cells through activation of the JNK signaling pathway. For the first time, this study provides new evidence of anti-HCC effects and mechanism of TB.

TB exerts anti-proliferative, pro-apoptotic, and tumor-inhibitory effects on Huh7 cells through activation of the JNK signaling pathway. For the first time, this study provides new evidence of anti-HCC effects and mechanism of TB.

Circular RNA (circRNA) has emerged as an important regulator in the progression of human diseases. However, the role of circRNAs in ovarian cancer remains largely unknown.

DNA sequencing and PCR were used to identify the existence and expression of circKRT7. The targeting relationship between circKRT7/miR-29a-3p and miR-29a-3p/COL1A1 was verified by fluorescence reporter assay. In vitro, colony formation, transwell and wound healing assay were used to detect the effects of circKRT7 and miR-29a-3p on the proliferation, migration and invasion ability of ovarian cancer cells. In vivo, xenograft tumor model was performed to validate the role of circKRT7 and miR-29a-3p in tumor growth.

We found that circKRT7 can promote the proliferation and metastasis of ovarian cancer cells by absorbing miR-29a-3p, which leads to the up-regulation of

. In vitro, knock-down of circKRT7 can inhibit the migration and invasion of ovarian cancer cells. This effect of circKRT7 is achieved by adsorbing miR-29a-3p and subsequently

release.