Dihydroartemisinin enhances the anti-tumor activity of oxaliplatin in colorectal cancer cells by altering PRDX2-reactive oxygen species-mediated multiple signaling pathways.

Background: Globally, colorectal cancer (CRC) is one of the leading causes of cancer-related deaths. Oxaliplatin based treatments are frequently used as chemotherapeutic methods for CRC, however, associated side effects and drug resistance often limit their clinical application. Dihydroartemisinin (DHA) induces apoptosis in various cancer cells by increasing reactive oxygen species (ROS) production.

Novel Regulatory Factors and Small-Molecule Inhibitors of FGFR4 in Cancer.

Fibroblast growth factor receptor 4 (FGFR4) is a tyrosine kinase receptor that is a member of the fibroblast growth factor receptor family and is stimulated by highly regulated ligand binding. Excessive expression of the receptor and its ligand, especially FGF19, occurs in many types of cancer. Abnormal FGFR4 production explains these cancer formations, and therefore, this receptor has emerged as a potential target for inhibiting cancer development.

Gracillin shows potent efficacy against colorectal cancer through inhibiting the STAT3 pathway.

Colorectal cancer (CRC) accounts for about 10% of all annually diagnosed cancers and cancer-related deaths worldwide. STAT3 plays a vital role in the occurrence and development of tumours. Gracillin has shown a significant antitumour activity in tumours, but its mechanism remains unknown.

miR-196b-5p-mediated downregulation of TSPAN12 and GATA6 promotes tumor progression in non-small cell lung cancer.

Lung cancer is the leading cause of cancer-related deaths worldwide and non-small cell lung cancer (NSCLC) accounts for over 80% of lung cancer cases. The RNA binding protein, QKI, belongs to the STAR family and plays tumor-suppressive functions in NSCLC. QKI-5 is a major isoform of QKIs and is predominantly expressed in NSCLC.

Curcumin derivative WZ35 inhibits tumor cell growth via ROS-YAP-JNK signaling pathway in breast cancer.

Background: Breast cancer is the most prevalent cancer among women worldwide. WZ35, an analog of curcumin, has been demonstrated to remarkably improve the pharmacokinetic profiles in vivo compared with curcumin. WZ35 exhibits promising antitumor activity in gastric cancer, HCC, colon cancer.

Alantolactone promotes ER stress-mediated apoptosis by inhibition of TrxR1 in triple-negative breast cancer cell lines and in a mouse model.

Triple-negative breast cancer (TNBC) is a subtype of breast cancer with poor clinical outcome and currently no effective targeted therapies are available. Alantolactone (ATL), a sesquiterpene lactone, has been shown to have potential anti-tumour activity against various cancer cells. However, the underlying mechanism and therapeutic effect of ATL in the TNBC are largely unknown.

[Recombinant adenovirus of microRNA-193b inhibits proliferation of K562 cells].

Objective: To construct a recombinant adenovirus vector containing human pre-miR-193b and investigate its effect on the proliferation of chronic myelocytic leukemia K562 cells.

Methods: The cDNA of pre-miR-193b was obtained by chemical synthesis and inserted into the adenoviral shuttle vector pAdTrack-CMV. The recombinant shuttle plasmid was linearized by Pme I and transformed into AdEasier cells for homologous recombination in E.

[Inhibitory effect of the recombinant adenovirus pre-miR-10a on K562 cell proliferation].

Aim: To investigate the changes of proliferation and apoptosis in K562 cells over-expressing miR-10a.

Methods: K562 cells were infected with pAd-pre-miR-10a virus, and then the levels of miR-10a and bcr/abl in transfected K562 cells was detected using RT-PCR and the level of BCR/ABL using Western blotting. The methylthiazolyl tetrazolium (MTT) assay and flow cytometry (FCM) were used to monitor the changes of proliferation and apoptosis of K562 cells after transfection.