var. 
  is an herb that possesses various ethnopharmacological applications. Herein, our current study focuses on the antitumor effect of a combination of physalins, which are regarded as the most representative secondary metabolites from calyces of 
  var. 
  .
 
  We mainly investigated the antitumor activity of the physalins extracted from 
  var. 
  on both solid and hematologic cancers. The main cells used in this study were NCI-H1975 and U266 cells. The major assays used were the CCK-8 assay, Western blot analyses, immunofluorescence assay and Annexin V assay, and a xenograft mouse model was used.
 
  The results showed that physalins exhibited a strong antitumoural effect on both non-small cell lung cancer (NSCLC) and multiple myeloma (MM) cells by suppressing constitutive STAT3 activity and further inhibiting the downstream target gene expression induced by STAT3 signaling, which resulted in the enhanced apoptosis of tumor cells.  https://www.selleckchem.com/products/fht-1015.html  Moreover, physalins significantly reduced tumor growth in xenograft models of lung cancer.
 
  Collectively, these findings demonstrated that the physalins from 
  var. 
  may potentially act as cancer preventive or chemotherapeutic agents for NSCLC and MM by inhibiting the STAT3 signaling pathway. The present study served as a promising guide to further explore the precise mechanism of 
  var. 
  in cancer treatment.
 Collectively, these findings demonstrated that the physalins from Physalis alkekengi var. franchetii may potentially act as cancer preventive or chemotherapeutic agents for NSCLC and MM by inhibiting the STAT3 signaling pathway. The present study served as a promising guide to further explore the precise mechanism of Physalis alkekengi var. franchetii in cancer treatment.
  In recent years, radioactive 
  I seed implantation combined with chemotherapy has been regarded as a safe and effective treatment for advanced non-small cell lung cancer (NSCLC). However, the mechanism underlying this success is still unclear.
 
  In this study, we investigated the apoptosis and anti-proliferative effect induced by 
  I in A549, H1975, and H157 cells and determined whether a sensitizing concentration of lobaplatin (LBP) could enhance these effects. We performed in vitro experiments on A549, H1975, and H157 cells; we investigated the effects of 
  I or lobaplatin (LBP) alone, or in combination, on cellular apoptosis and proliferation by performing flow cytometry, Bax/Bcl2 ratio, TUNEL, cell viability assay, cell cycle, and EdU. To further verify our findings, a subcutaneous tumor mouse model was established. Moreover, AKT/mTOR pathway was detected to determine whether this pathway was involved in the anti-cancer effect of 
  I and LBP by up-regulating or down-regulating the expression of mTOR.
 
  Based on our results, the sensitizing concentration of LBP could enhance the 
  I-induced apoptosis and anti-proliferation effect. Furthermore, the subcutaneous tumor mouse model obtained the consistent results. More importantly, the AKT/mTOR pathway was down-regulated after the treatment of 
  I and LBP, and the anti-cancer effect of 
  I and LBP could be compromised by up-regulating the mTOR expression.
 
  Our study proved that LBP promotes the apoptotic and anti-proliferative effects of 
  I in NSCLC cells by inhibiting the AKT/mTOR pathway and provides a foundation for future studies and enhanced combinatorial approaches for NSCLC in the clinical setting.
 Our study proved that LBP promotes the apoptotic and anti-proliferative effects of 125I in NSCLC cells by inhibiting the AKT/mTOR pathway and provides a foundation for future studies and enhanced combinatorial approaches for NSCLC in the clinical setting.
  Growth arrest and DNA-damage-inducible 45 beta (
  ) is overexpressed and is associated with poor clinical outcomes in many human cancers, but the clinical implication of 
  in epithelial ovarian cancer (EOC) remains unclear.
 
  Bioinformatics analysis of The Cancer Genome Atlas (TCGA) and gene expression omnibus (GEO) cohorts was used to illustrate the relationship between 
  expression and metastasis, as well as the survival time of EOC. 
  was downregulated by siRNAs in EOC cells, and migration ability was determined by a transwell assay and wound-healing assay. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and gene set enrichment analysis (GSEA) were conducted to discover the downstream pathway of 
  . The regulation of epithelial-mesenchymal transition (EMT) by GADD45B was verified by Western blotting and qRT-PCR. Finally, the correlation of 
  expression with EOC metastasis was investigated in EOC tissues by immunohistochemistry.
 
  Overexpression of 
  indicates shorter overate the motility of ovarian cancer cells through EMT, is associated with EOC metastasis, and may be a new biomarker of metastasis and prognosis.[This corrects the article DOI 10.2147/OTT.S258896.].
  Cellular senescence is a physiological phenomenon by which cells irreversibly lose their proliferative potential. It is not clear whether senescent cells are related to malignant transformation in oral precancerous lesions. The role of peroxiredoxin1 (Prx1)-induced cell senescence in OLK malignant transformation has not been reported. The aim of this study is to investigate the role and mechanism of cell senescence in oral carcinogenesis.
 
  In this study, 4-nitro-quinoline-1-oxide (4NQO) induced tongue carcinogenesis model in Prx1
  and Prx1
  mice and dysplastic oral keratinocyte (DOK) were used. Prx1 knockdown DOK cells were harvested with shRNA injection, and cell senescence was detected via the senescence-associated β-galactosidase (SA β-gal) assay. The senescence and mitophagy-related proteins were observed by immunohistochemistry (IHC), Western blot and qRT-PCR. The binding of Prx1 with prohibitin 2 (PHB2) and light chain 3 (LC3) was predicted via ZDOCK and measured in mice by Duolink analysis.
 
  Histologically, 4NQO treatment induced epithelial hyperplasia, dysplasia (mild, moderate and severe), carcinomas in situ and oral squamous cell carcinoma (OSCC) in mouse tongue mucosa. The malignant transformation rate in Prx1
  mice (37.5%) was significantly lower compared with Prx1
  mice (57.1%). In Prx1
  mice, a higher number of senescent cells and greater expression of p53 and p21 were observed in hyperplastic and dysplastic tongue tissues when compared with those in OSCC tissues. Prx1 knockdown induced a greater number of senescent cells in hyperplastic tissues, and DOK cells accompanied cell cycle arrest at the G1 phase and PHB2/LC3II downregulation. Prx1 was predicted to dock with PHB2 and LC3 via ZDOCK, and the interactions were confirmed by in situ Duolink analysis.
 
  Prx1 silencing inhibits the oral carcinogenesis by inducing cell senescence dependent on mitophagy.
 Prx1 silencing inhibits the oral carcinogenesis by inducing cell senescence dependent on mitophagy.