RANKL Promotes Chemotherapy Resistance in Breast Cancer Cells Through STAT3 Mediated Autophagy Induction.

Background: This study was to investigate the functional role and mechanism of receptor activator of nuclear factor-kappa B ligand (RANKL) associated autophagy and chemoresistance in breast cancer.

Materials And Methods: Cell Counting Kit-8 (CCK-8) assay was used to detect the cell viability. Real-time polymerase chain reaction (PCR) was used for determining the relative mRNA levels of key genes and protein expression was assessed by Western blotting.

A rare presentation of a large goiter with papillary thyroid microcarcinoma as a chest wall mass: A case report.

Nodular goiter affects numerous individuals worldwide. As the thyroid enlarges, it normally extends into the mediastinum as a result of its anatomical location under the investing layer of the deep cervical fascia. The present study reports the rare case of a 76-year-old man who suffered from a goiter with papillary thyroid microcarcinoma, who presented as a subcutaneous partially cystic with solid areas lesion over the chest.

RANKL-induced migration of MDA-MB-231 human breast cancer cells via Src and MAPK activation.

Accumulating studies have shown that the receptor activator of nuclear factor-κB ligand (RANKL)/RANK pathway plays an important role in tumor metastasis. However, the involvement of the RANKL/RANK signal transduction pathway in breast cancer metastasis remains unclear. The present study, therefore, investigated the role of downstream molecules of RANKL/RANK signaling in breast cancer cells using Transwell chemotaxis assays.

Hypoxia induces RANK and RANKL expression by activating HIF-1α in breast cancer cells.

Receptor activator of NF-κB (RANK) and RANK ligand (RANKL) are known to play an important role in the development and progression of breast cancer. However, the mechanisms by which stimuli regulate the expression of RANK and RANKL in breast cancer cells are largely unknown. In this study, we show that hypoxia, a common feature of malignant tumors, can enhance the expression of RANK and RANKL mRNA and protein in MDA-MB-231 and MCF-7 breast cancer cells.