Resveratrol is a representative polyphenol of diet-derived putative cancer chemopreventive agents, which have attracted increasing interest in the cancer chemoprevention community. The inhibition of the action of human papillomavirus (HPV) E6 and E7 has been considered a key approach for cervical cancer therapy. Resveratrol has been shown to induce the apoptosis, and reduce both the viability and mitotic index of a number of cancer cell lines, including human cervical cancer cells. In the present study, it was confirmed that resveratrol inhibited the HPV E6 mRNA, HPV E6 protein and phosphorylated retinoblastoma protein (p-pRb1) levels, and increased the p53 protein levels in HeLa and Ca Ski cells, as well as in subcutaneous tumor tissue grown from HeLa cells. High-risk HPV uses a bicistronic RNA to control E6 and E7 genes simultaneously. On the whole, the present study demonstrates that resveratrol inhibits cervical cancer development by suppressing the transcription and translation of E6 and E7, and also by promoting the apoptosis and G1/S phase transition arrest. These findings may provide the basis for the development of resveratrol as a candidate for cervical cancer therapy.
Background Hereditary spherocytosis (HS) is the most common haemolytic anaemia caused by congenital membrane defects of red blood cells. The name derives from the presence of spherical red blood cells in the peripheral blood. Clinical manifestations of HS are anaemia, haemolytic jaundice, and large spleen, and infection can worsen the condition, often with cholelithiasis. HS is mainly caused by abnormal functions of the products of six genes. Splenectomy is the main treatment for HS. Case presentation Half a day after birth, the proband exhibited HS-related symptoms, with progressive aggravation. Routine examination in the outpatient department showed an increase in white blood cells and a decrease in red blood cells. His mother had HS and a partial splenectomy. We suspected that the infant might also have HS. Genomic DNA samples were extracted from the three members of the HS trio pedigree, and genomic whole-exome sequencing (WES) was performed. The three DNA samples were amplified by polymerase chain reaction (PCR), followed by Sanger sequencing to identify mutation sites. A novel nonsense heterozygous mutation, c.790C > T (p. Gln264Ter), in the ANK1 gene, which causes premature termination of translation, was found in this Chinese family with autosomal dominant HS. Conclusions This de novo nonsense mutation can cause the onset of HS in early childhood, with severe symptoms. Expanding the ANK1 genotype mutation spectrum will lay a foundation for the further application of mutation screening in genetic counselling.
Raman spectroscopy (RS) has been used in clinical diagnostics, tissue engineering, and toxicology experiments owing to its label‐free, low‐destructive, high sensitivity, and strong specificity. Nonetheless, their application has been limited because of the integrated analysis of biological experimental methods and RS. In this study, it was challenged that applied RS in combination with biological experiments to distinguish colorectal cancer (CC) cells from which treated with artesunate (ART), which has obvious antitumor effects. Heavy water (D2O) was used to detect changes in colorectal cancer cell metabolism. The Raman spectral intensity of the C–D band at 2100–2300 cm−1 was significantly weakened in CC (SW480, SW620, and HCT116) treated with ART. According to the CCK‐8, wound healing, and Transwell assays, the activity of SW480 and SW620 cells was significantly inhibited by ART. Through literature tracking and transcriptome sequencing, multiple signal pathways of SW480 and SW620 cells have changed significantly after treatment with ART, such as “apoptotic signaling pathway,” “cell cycle phase transition,” “mitochondrial part,” and “mRNA metabolic process.” The Raman peak area significantly decreased at 490 cm−1, 746 cm−1, 1126 cm−1, 1311 cm−1, 1337 cm−1, and 1582 cm−1 in SW480 and SW620 cells treated with ART. It showed that these Raman bands are associated with ART‐induced apoptosis‐related signaling pathways. In addition, we found that application of the RS in cell type identification will be prosperous. By integrating RS with biological mechanisms, its application in the biomedical field is increasing, and its significance in biological sample detection has become more prominent.
Background: Hirschsprung's disease (HSCR) caused by absence or dysfunction of ganglion cells in the submucosal plexus and intermuscular plexus of the intestinal wall. Studies have shown that homozygous mutations of glial cell-line derived neurotrophic factor ( GDNF ) can lead to the occurrence of HSCR. but heterozygous mutation must combine with other related abnormal genes could to cause the HSCR. The other Guanylyl cyclase C ( GUCY2C ) gene is rarely reported as a direct cause of HSCR. Our findings Provides a new perspective for application of mutation screening in the genetic counseling.Case presentation: We report clinical and genetic findings of a trio pedigree with Hirschsprung's disease. Whole exome sequencing and Sanger sequencing were performed for propositus and all members of trio pedigree, respectively. We also collected 74 healthy control samples and used Sanger sequencing to identify that found the mutation. We first described the rare trio pedigree of HSCR caused by two special genes of GDNF (p.Arg93Gln) and GUCY2C (p.Tyr1072Cys). Studies have found that mutations in GDNF alone do not cause HSCR symptom, so is propositus’ mother in this study. Common mutation of GDNF gene mutation inherited from mother of proband, but the rare mutation of GUCY2C from the father. None of the parents showed HSCR phenotype. We provide evidence for the causative role of the two variants.Conclusions: Our study found that GDNF and GUCY2C together lead to the occurrence of HSCR. This finding expands the genotype spectrum and increases knowledge on the genetic molecular mechanisms of the HSCR. Our findings will provide help for the screening of pathogenic genes of HSCR.
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