Correction to "Rapamycin Inhibits Osteoclastogenesis and Prevents LPS-Induced Alveolar Bone Loss by Oxidative Stress Suppression".

[This corrects the article DOI: 10.1021/acsomega.3c01289.

Rapamycin Inhibits Osteoclastogenesis and Prevents LPS-Induced Alveolar Bone Loss by Oxidative Stress Suppression.

Periodontitis is a progressive inflammatory skeletal disease characterized by periodontal tissue destruction, alveolar bone resorption, and tooth loss. Chronic inflammatory response and excessive osteoclastogenesis play essential roles in periodontitis progression. Unfortunately, the pathogenesis that contributes to periodontitis remains unclear.

Tamoxifen represses miR-200 microRNAs and promotes epithelial-to-mesenchymal transition by up-regulating c-Myc in endometrial carcinoma cell lines.

Although tamoxifen (TAM), a selective estrogen receptor modulator, has been widely used in the treatment of hormone-responsive breast cancer, its estrogen-like effect increases the risk of endometrial cancer. However, the molecular mechanisms of TAM-induced endometrial carcinoma still remain unclear. In this report, we explored the role of microRNAs (miRNAs) in TAM-induced epithelial-mesenchymal transition (EMT) in ECC-1 and Ishikawa endometrial cancer cell lines and found miR-200 is involved in this process via the regulation of c-Myc.

TSA suppresses miR-106b-93-25 cluster expression through downregulation of MYC and inhibits proliferation and induces apoptosis in human EMC.

Histone deacetylase (HDAC) inhibitors are emerging as a novel class of anti-tumor agents and have manifested the ability to decrease proliferation and increase apoptosis in different cancer cells. A significant number of genes have been identified as potential effectors responsible for the anti-tumor function of HDAC inhibitor. However, the molecular mechanisms of these HDAC inhibitors in this process remain largely undefined.

Estrogen-induced dimerization and activation of ERα-fused caspase-8: artificial reversal of the estrogenic hormone effect in carcinogenesis.

The cascade of caspase processing and activation is the core of apoptotic cell signaling. Initiator caspases are activated by adaptor-mediated clustering, which allows the intermolecular autoprocessing of the zymogens in close proximity. Caspase-8, the prototypical initiator critically involved in apoptosis induced by varied extrinsic stimuli, is physiologically recruited via a classical FasL/Fas/FADD pathway.

Ibandronate promotes osteogenic differentiation of periodontal ligament stem cells by regulating the expression of microRNAs.

Bisphosphonates (BPs) have a profound effect on bone resorption and are widely used to treat osteoclast-mediated bone diseases. They suppress bone resorption by inhibiting the activity of mature osteoclasts and/or the formation of new osteoclasts. Osteoblasts may be an alternative target for BPs.

[Expression of a chimeric gene containing poly-arginine as the protein transduction domain and its killing activity against HER2 positive gastric cancer SGC-7901 cells].

Aim: To construct a eukaryotic expression vector for chimeric gene containing poly-arginine as the protein transduction domain(PTD) and transiently transfect this vector into HER2 positive SGC-7901 cells and HER2 negative HeLa cells to examine its effect on cell growth.

Methods: PCR amplication was used to obtain the gene of active form caspase-3 fused with nonaarginine, and then fusion gene was cloned into eukaryotic expression vector containing e23sFv DNA fragment. After this chimeric gene transfected into SGC-7901 cells and HeLa cells by Lipofectamine 2000™; reagent, indirect immunofluorescence and cell counting were used to examine the expression in these two cells and the effect on cell growth.