Vistisenbanke3588

RNF128 promotes HCC progression by activating EGFR/MEK/ERK signaling pathway, which might function as a novel prognostic molecular signature with the potential to be a candidate therapeutic target for HCC patients.

RNF128 promotes HCC progression by activating EGFR/MEK/ERK signaling pathway, which might function as a novel prognostic molecular signature with the potential to be a candidate therapeutic target for HCC patients.Pulmonary pleomorphic carcinoma (PPC) generally lacks actionable driver mutations such as epidermal growth factor receptor mutations or anaplastic lymphoma kinase or c-ros oncogene 1 (ROS1) rearrangements. The response to crizotinib, ceritinib, brigatinib, and lorlatinib in ROS1-positive advanced non-small cell lung carcinoma is well established; however, there is little mention of their successful administration in pulmonary pleomorphic carcinoma cases. We report a case of a stage II PPC with recurrence after surgical resection and developed multiple distant metastasis. The tumor was refractory to chemotherapy and immunotherapy with progressive disease. EZR-ROS1 fusion was detected by next-generation sequencing and showed a good response to serial ROS1 inhibitors combined with surgery and radiotherapy. Now under lorlatinib, all her lesions responded well during the follow-up with sustained partial remission for more than 18 months. A sustainable treatment effect can be achieved in pulmonary pleomorphic carcinoma with driver mutations with tyrosine kinase inhibitor treatment. Driver mutations should be regularly tested in pulmonary pleomorphic carcinomas.

Breast cancer exhibits poor prognosis and high relapse rates following chemotherapy therapeutics. Thus, this study aims to develop effective novel agents regulating the core molecular pathway of breast cancer such as Wnt/β-catenin signaling.

The present study screened a novel inhibitor, called "C188", using MTT assay. The molecular formula of C188 is C

H

FN

O

and the molecular weight is 390. Flow cytometry and Western blotting were employed to assess cell cycle arrest after treatment with C188. Wound-healing and transwell assays were applied to measure the cell migration and invasion viability. The regulatory effects of C188 on Wnt/β‑catenin signaling and localization of β‑catenin in the nucleus were investigated by Western blotting and immunofluorescence.

We found that C188 significantly suppressed proliferation and growth in a dose- and time-dependent manner in breast cancer cells, but not in normal breast cells. The inhibitory effect was caused by cell cycle arrest at the G1-phase which is induced by C188 treatment. Additionally, C188 dramatically inhibited cell migration of breast cancer cells in a dose-dependent manner. The migration inhibition was attributed to the suppression of Wnt/β‑catenin signaling and localization of β‑catenin in the nucleus mediated by regulating phosphorylation of β‑catenin and its subsequent stability. Furthermore, the target genes, including

,

, and

, were downregulated due to the decrease of β‑catenin in the nucleus after exposure to C188.

C188 treatment resulted in the downregulation of cyclin D which led to cell cycle arrest at the G1 phase, and the inhibition of cell migration, indicating that C188 may be an effective novel therapeutic candidate as a potential treatment for human breast cancer.

C188 treatment resulted in the downregulation of cyclin D which led to cell cycle arrest at the G1 phase, and the inhibition of cell migration, indicating that C188 may be an effective novel therapeutic candidate as a potential treatment for human breast cancer.

Cutaneous squamous cell carcinoma (cSCC) is the most common second basal cell carcinoma in our population. Wogonoside, the main in vivo metabolite of wogonin, possesses anti-inflammatory, anti-angiogenesis and anti-cancer activities. Nevertheless, the effectiveness of wogonoside therapy on cSCC has not been clarified.

In this study, we investigated the effects of wogonoside on cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and cancer stem-like cell (CSC) properties of SCL-1 and SCC12 cell lines, and the effects on tumor formation in vivo. In vitro, cells were treated with 0, 25, 50 and 100 μM wogonoside for 48 h. In vivo, SCL-1 cells were subcutaneously injected into the right thigh of mice to form xenograft tumors. Animals were randomly divided into two groups (n=10) the control group and the 80 mg/kg wogonoside group.

The results showed that wogonoside attenuated proliferation, invasion and EMT of SCL-1 and SCC12 cell lines, and enhanced the rate of apoptosis. Meanwhile, wogonostion and cancer intervention.

Glioma (GM) is a common type of malignant and aggressive tumor in brain with poor prognosis. Circular RNAs (circRNAs) are well-known regulators in cancer progression. However, its molecular basis in GM remains to be investigated.

CircRNA microarray was used to detect differentially expressed circRNAs in GM and matched noncancerous tissues. qRT-PCR was applied to detect the expression profile of circ-ELF2 in GM tissue specimens and cell lines. CCK-8, clone formation, AO/EB staining, flow cytometry, wound healing, and transwell assays were performed to identify the functions of circ-ELF2 in GM cells. The distribution of circ-ELF2 was analyzed by RNA-FISH and subcellular fractionation assay. Dual-luciferase reporter assay was applied to verify the predicted binding sites between miR-510-5p and circ-ELF2/MUC15 3'-UTR. Rescue assay was finally conducted to explore whether the oncogenic role of circ-ELF2 was partially attributed to miR-510-5p/MUC15 signaling.

We observed that circ-ELF2 was significantly upregulated in GM tissues, which was analyzed by circRNA microarray and qRT-PCR. Upregulation of circ-ELF2 was associated with poor prognosis and high recurrence rate for GM patients after surgery. The collapse of circ-ELF2 caused growth arrest and downregulation of cell migratory and invasive potential of GM cells and promoted cell apoptosis. PI3K inhibitor In contrast, elevated expression of circ-ELF2 led to the opposite effect. Mechanistically, circ-ELF2 acted as a competing endogenous RNA (ceRNA) for miR-510-5p to positive modulate MUC15 expression at posttranscriptional level. Circ-ELF2 upregulated MUC15 by sponging miR-510-5p, thus promoting GM growth and aggressiveness.

This study indicates that circ-ELF2/miR-510-5p/MUC15 signaling plays a key role in promoting the occurrence and development of GM.

This study indicates that circ-ELF2/miR-510-5p/MUC15 signaling plays a key role in promoting the occurrence and development of GM.