syedzayyan/paper_mill_benchmark huggingface dataset:
Hispidulin suppresses cell growth and metastasis by targeting PIM 1 through JAK 2/STAT 3 signaling in colorectal cancer

Colorectal cancer ( crc ) accounts for over 600 000 deaths annually worldwide.The current study aims to evaluate the value of proto‐oncogene pim 1 as a therapeutic target in crc and investigate the anticancer activity of hispidulin, a naturally occurring phenolic flavonoid compound, against crc .Immunohistochemistry analysis showed that pim 1 was upregulated in crc tissue.The role of pim 1 as an oncogene was evidenced by the fact that pim 1 knockdown inhibits cell growth, induces apoptosis, and suppresses invasion.Our results showed that hispidulin exerts antitumor activity in crc through inhibiting the expression of pim 1 .Moreover, our findings revealed that hispidulin downregulated the expression of pim 1 by inhibiting jak 2/ stat 3 signaling by generating reactive oxygen species.Furthermore, our in vivo studies showed that hispidulin can significantly inhibit tumor growth and metastasis in crc .Collectively, our results provide an experimental basis for trialing hispidulin in crc treatment.Pim 1 can be considered a potential therapeutic target in crc .

Journal: Cancer Science (2018)
Publication types: Research Article;
Downregulation of microRNA-1469 promotes the development of breast cancer via targeting HOXA1 and activating PTEN/PI3K/AKT and Wnt/ß-catenin pathways

Breast cancer (bc) is a common malignancy which is the most frequently diagnosed cancer in women all over the worldwide.This study aimed to investigate the roles of mi r‐1469 in the development of bc, as well as its regulatory mechanism.The expression levels of mi r‐1469 in bc tissues, serum, and cell lines were determined.Effects of overexpression of mi r‐1469 on mcf7 cell viability, colony‐forming ability, apoptosis, migration, and invasion were then investigated.Furthermore, the potential target of mi r‐1469 in mcf7 cells was explored.Besides, the association between mi r‐1469, pten/pi3k/akt, and wnt/β‐catenin pathways was elucidated.Notably, confirmatory experiments by downregulation of mi r‐1469 in sk‐br‐3 cells were further performed.The mi r‐1469 expression was significantly downregulated in bc tissues, serum, and cell lines.The overexpression of mi r‐1469 significantly inhibited the proliferation, arrested cell‐cycle at g2/m phase, increased apoptosis, suppressed migration, and invasion of mcf‐7 cells.In addition, hoxa1 was verified as a direct target of mi r‐1469, and the effects of overexpression of mi r‐1469 on the malignant behaviors of mcf7 cells were significantly counteracted by overexpression of hoxa1 concurrently.Furthermore, the overexpression of mi r‐1469 suppressed the activation of pten/pi3k/akt and wnt/β‐catenin pathways, which was reversed overexpression of hoxa1 concurrently.Besides, confirmatory experiments showed that the inhibition of mi r‐1469 promoted the malignant behaviors of sk‐br‐3 cells, which was inversed after mi r‐1469 inhibition and hoxa1 knockdown at the same time.Our findings reveal that downregulation of mi r‐1469 may promote the development of bc by targeting hoxa1 and activating pten/pi3k/akt and wnt/β‐catenin pathways.Mi r‐1469 may serve as a promising target for bc therapy.

Journal: Journal of Cellular Biochemistry (2018)
Publication types: Research Article;
Sinomenine exerts antitumour effect in gastric cancer cells via enhancement of miR-204 expression

Gastric carcinoma (gc) is a pernicious neoplasm with high morbidity and mortality.Sinomenine (sin) has long been exploited to heal rheumatoid arthritis.Recently, sin has been discovered to exert the antitumour functions in diverse cancers.However, the impacts of sin on gc remain indistinct.We attempted to expose the antitumour effect of sin on gc.Mkn45 and sgc‐7901 cells were administered with sin for 24 hours, cell viability, proliferation, apoptosis, migration, invasion and the associated proteins in the above processes were examined via exploiting cck‐8, brd u, flow cytometry, transwell and western blot.Mi r‐204 expression in gc tumour tissues, different gc cell lines and sin‐stimulated gc cells was investigated by executing rt‐q pcr.The above cell biological processes were reassessed after transfection with mi r‐204 inhibitor.The latent mechanisms were probed by examining ampk and wnt/β‐catenin pathways.We found that sin memorably repressed cell proliferation, evoked apoptosis and affected cyclin d1, bcl‐2, bax and cleaved‐caspase‐3 expression in mkn45 and sgc‐7901 cells.Cell migration, invasion and expression of mmp‐9 and vimentin were all restrained by sin stimulation.The increase of mi r‐204 was discovered in gc tissues and sin‐treated mkn45 and sgc‐7901 cells.But suppression of mi r‐204 was observed in ags, mkn28, mkn45 and sgc‐7901 cells.Suppression of mi r‐204 overturned the inhibitory functions of sin in mkn45 and sgc‐7901 cells.Besides, sin prohibited ampk and wnt/β‐catenin pathways via enhancement of mi r‐204.In conclusion, these findings suggested that sin exerted the antitumour activity in gc cells by hindering ampk and wnt/β‐catenin pathways via enhancement of mi r‐204.

Journal: Basic & Clinical Pharmacology & Toxicology (2019)
Publication types: Research Article;