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Objective: To explore the therapeutic effect of naringin on colorectal cancer (CRC) and the related mechanism. Methods: Cell counting kit-8 (CCK-8) assay and annexin V-FITC/PI assay were used to detect the effect of naringin (50–400 µg/mL) on cell proliferation and apoptosis of CRC cells, respectively. The scratch wound assay and transwell migration assay were used to assess the effect of naringin on CRC cell migration. Four-week-old male nude mice were injected with HCT116 cells subcutaneously to establish the tumor xenograft model. Naringin was injected intraperitoneally at 50 mg/(kg·d), with solvent and 5-fluorouracil treatment as control. The width and length of the tumors were measured and recorded every 6 days, and tumor tissues were photographed and weighed on the last day of the 24-d observation period. Immunohistochemical staining for caspase-3, proliferating cell nuclear antigen and TUNEL assay were used to evaluate the effect of naringin on cell proliferation and apoptosis in tumor tissues. The body weight, food and water intake of mice were recorded, and the major organs in different treatment groups were weighed on the last day and stained with hematoxylin and eosin for histological analysis. Meanwhile, the routine blood indicators were recorded. Results: CCK-8 and annexin V-FITC/PI results confirmed that naringin (100, 200, and 400 µg/mL) could inhibit proliferation and promote apoptosis. The scratch wound assay and transwell migration assay results confirmed the inhibitory activity of naringin against CRC cells migration. In vivo results demonstrated the inhibitory effect of naringin on tumor growth with good bio-compatibility. Conclusion: Naringin inhibited colorectal carcinogenesis by inhibiting viability of CRC cells. [ABSTRACT FROM AUTHOR]

Hypercholesterolemia can aggravate contrast‐induced acute kidney injury, and the exacerbation of renal tubular epithelial cell (RTEC) injury is a major cause. However, the exact mechanisms remain obscure. Mitophagy, a type of autophagy, selectively eliminates damaged mitochondria and reduces mitochondrial oxidative stress, which is strongly implicated in cell homeostasis and acute kidney injury. Oxidized low‐density lipoprotein (Ox‐LDL) is accumulated in hypercholesterolemia and has a cytotoxic effect. This study aimed to determine whether and how ox‐LDL exacerbates contrast‐induced injury in RTECs and to further explore whether PINK1/Parkin‐dependent mitophagy is involved in this process. Iohexol and ox‐LDL were used alone or in combination to treat HK‐2 cells. Rapamycin pretreatment was utilized to enhance mitophagy. Cell viability, apoptosis, mitochondrial membrane potential (MMP) and mitochondrial reactive oxygen species (mtROS) were detected by cell counting kit‐8, TUNEL staining, JC‐1 kit and MitoSOX fluorescence, respectively. The expression of mitophagy‐related proteins (including PINK1, Parkin, and so on) and cleaved caspase‐3 was confirmed by western blot. Colocalization of MitoTracker‐labeled mitochondria and LysoTracker‐labeled lysosomes was observed by fluorescence microscopy to evaluate mitophagy. The results of our study showed that ox‐LDL aggravated MMP decline, mtROS release and apoptosis in iohexol‐treated HK‐2 cells, accompanied by a further increased autophagy level. Enhancement of PINK1/Parkin‐dependent mitophagy by rapamycin alleviated apoptosis and mitochondrial injury in HK‐2 cells in response to iohexol under ox‐LDL condition. Therefore, our findings indicate that ox‐LDL aggravates contrast‐induced injury of RTECs by increasing mitochondrial damage and mitochondrial oxidative stress, which may be associated with the relative insufficiency of PINK1/Parkin‐dependent mitophagy. [ABSTRACT FROM AUTHOR]

Bladder cancer is a common tumour of the urinary system, and more than 90% is urothelial carcinoma. Therefore, it is important for discovering the key target genes and molecules of bladder tumour cell metastasis and invasion. Our research initially explored the regulation of deltaN p63 on the progression and metastasis of bladder cancer and found that deltaN p63 can influence the occurrence of EMT through PTEN and ultimately regulate the growth and metastasis of bladder cancer. In summary, this study identified a new EMT regulator, deltaN p63, further revealed the mechanism of the invasion and metastasis of bladder cancer cells, and provided a theoretical basis for finding new target molecules and drugs to treat bladder cancer. In conclusion, this study will further reveal the mechanism of tumour cell invasion and metastasis and provide a theoretical basis for cancer treatment to find new target molecules and drugs. [ABSTRACT FROM AUTHOR]