Articles written in Journal of Biosciences
Volume 42 Issue 3 September 2017 pp 405-416 Article
Knockdown of Cripto-1 inhibits the proliferation, migration, invasion, and angiogenesis in prostate carcinoma cells
DING WU ZHAN SHI HAO XU RENFU CHEN SONG XUE XIAOQING SUN
Cripto-1 (CR-1) is a member of the epidermal growth factor-Cripto-1/FRL1/Cryptic gene family that plays a key role in thevarious malignant cancers. However, the role of CR-1 in prostate carcinoma (PCa) remains limited. The expression of CR-1was down-regulated by small interfering RNA (siRNA). Western blot measured the expression levels of CR-1 and somerelated proteins. We performed Cell Counting Kit-8, 5-ethynyl-2-deoxyuridine (EdU) incorporation assay and flowcytometry to detect the cellular proliferation and cycle. The transwell assay was used to observe cellular migration andinvasion. The ability of angiogenesis was evaluated by tube formation assay. Our results showed that CR-1 knockdownmarkedly inhibited cell proliferation and induced cycle arrest in G1 phase, as p21 and p27 were up-regulated, whereascyclin D1 and cyclin E1 were diminished. Moreover, silencing of CR-1 dramatically inhibited cell migration and invasion,repressed matrix metalloproteinases, and disturbed epithelial-mesenchymal transition. CR-1 siRNA suppressed the secretedlevel of vascular endothelial growth factor, and reduced protein level of Vascular endothelial growth factor receptor 2. Wefurther found that decreased CR-1 expression inhibited FAK/Src/PI3K and Wnt/b-catenin signalling in PCa cells. Theseresults suggested CR-1 might be served as an effective therapeutic target in PCa.
Volume 42 Issue 3 September 2017 pp 491-499 Article
Hypoxia stimulates invasion and migration of human cervical cancer cell lines HeLa/SiHa through the Rab11 trafficking of integrin αvβ3/FAK/PI3K pathway-mediated Rac1 activation
HAO XU YUAN YUAN WENQIAN WU MIN ZHOU QIAN JIANG LINJUN NIU JIAYIN JI NIANLI LIU LONGZHEN ZHANG XIA WANG
Hypoxia plays a key role in tumour cell survival, invasion, and metastasis. An increasing number of studies have attemptedto characterize the tumour response to hypoxia and to identify predictive markers of disease. Here we show that hypoxiaincreases tumour cell invasion and migration by the modulation of Rab11, an important molecule for vesicular trafficking.In our study, we found that Rab11, together with the activation of Rac1, could stimulate invasion and migration of cervicalcancer cell lines HeLa/SiHa in hypoxia. Activation of Rac1 activity by hypoxia seems to be central to carcinoma invasion.We also found that these effects could be related to the integrin αvβ3. In addition, we studied the molecular pathway for thisprocess. Our results showed that in cervical cancer cell lines HeLa/SiHa, Rac1 activation in hypoxia could stimulateinvasion and migration, and this process was mediated by integrin αvβ3-mediated FAK and PI3K phosphorylation.Furthermore, hypoxia induced a dramatic increase in αvβ3 integrin surface expression, and this increase is dependent onRab11. In conclusion, our study might provide a new mechanism for the effect of hypoxia on stimulating cervicalcarcinoma invasion.
Volume 45 All articles Published: 12 February 2020 Article ID 0040 Article
Silencing of HOXB9 suppresses cellular proliferation, angiogenesis, migration and invasion of prostate cancer cells
HAO XU SHANGJUN WU XIN SHEN DING WU ZHENGUO QIN HAO WANG XIAOGANG CHEN XIAOQING SUN
The Homeobox B9 (HOXB9) is a homeodomain-containing transcription factor that participates in the progressionof various malignancies. Nevertheless, the functional role of HOXB9 in prostate cancer cells is largelyunknown. Hence, we aimed to address the effect of HOXB9 on the progression of prostate cancer cells. Smallinterfering RNA (siRNA) against HOXB9 was used to downregulate HOXB9 expression in PC3 and DU145cells. Western blotting was performed to detect the expression levels of HOXB9 and other related proteins. Cellproliferation was tested by the Cell Counting Kit-8 (CCK-8) and cell cycle and apoptosis were investigated byflow cytometry. Angiogenesis was examined using tube formation assays The Transwell assays were carriedout to assess the migratory and invasive capacities of cells. Here, we found that HOXB9 knockdown significantlyreduced cell proliferation via inducing cell cycle arrest at G1 phase. This treatment also reducedangiogenesis, migration and invasion abilities of PC3 and DU145 cells in vitro. We also found that HOXB9knockdown inhibits the activation of the PI3K/AKT signaling pathway in prostate cancer cells. In conclusion,our findings revealed that HOXB9 promotes prostate cancer progression and might be a novel and effectivetherapeutic target for human prostate cancer.
Volume 46 All articles Published: 4 December 2021 Article ID 0113 Article
17 β-Estradiol alleviates oxidative damage in osteoblasts by regulating miR-320/RUNX2 signaling pathway
YANYAN XU HAO XU XIUPING YIN XIANLI LIU ZHONGXI MA ZHIGANG ZHAO
The aim of this study is to investigate the effect and mechanism of 17 beta-estradiol (E2) on oxidative stress in theosteoblasts. An oxidative stress-induced damage model was established using H2O2 in MC3T3-E1 cells, andH2O2-induced cells were treated with E2. The results indicated that E2 attenuated oxidative stress in H2O2-induced MC3T3-E1 cells. In addition, H2O2 upregulated the expression of miR-320-3p and downregulated thatof RUNX2, but these changes were counteracted by E2. Thereafter, we verified the interactive relationshipbetween miR-320-3p and RUNX2. Then, H2O2-induced MC3T3-E1 cells were transfected with miR-320-3pmimics or inhibitors and treated with E2. The results indicated that miR-320-3p inhibition suppressed H2O2-induced inflammation, apoptosis, and oxidative stress and promoted the osteogenic differentiation of MC3T3-E1 cells by regulating RUNX2, ALP, and OCN, and this effect was further strengthened by E2. In conclusion,the findings suggest that E2 alleviates oxidative damage in osteoblasts by regulating the miR-320/RUNX2signaling.
Volume 48, 2023
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