scholarly journals Gynura procumbens ethanolic extract suppresses osteosarcoma cell proliferation and metastasis in vitro

2013 ◽  
Vol 6 (1) ◽  
pp. 113-117 ◽  
Author(s):  
HENG WANG ◽  
JI WEN ZHOU ◽  
DA HUA FU ◽  
YANG ZHOU ◽  
WEN ZHAO CHENG ◽  
...  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zehua Zhang ◽  
Fei Dai ◽  
Fei Luo ◽  
Wenjie Wu ◽  
Shuai Zhang ◽  
...  

AbstractOsteosarcoma is a malignant osteoblastic tumor that can gravely endanger the lives and health of children and adolescents. Therefore, there is an urgent need to explore new biomarkers for osteosarcoma and determine new targeted therapies to improve the efficacy of osteosarcoma treatment. Diaphanous related formin 3 (DIAPH3) promotes tumorigenesis in hepatocellular carcinoma and lung adenocarcinoma, suggesting that DIAPH3 may be a target for tumor therapy. To date, there have been no reports on the function of DIAPH3 in osteosarcoma. DIAPH3 protein expression in osteosarcoma tissues and healthy bone tissues adjacent to cancer cells was examined by immunohistochemical staining. DIAPH3 mRNA expression correlates with overall survival and reduced disease-free survival. DIAPH3 protein is upregulated in osteosarcoma tissues, and its expression is significantly associated with tumor size, tumor stage, node metastasis, and distant metastasis. Functional in vitro experiments revealed that DIAPH3 knockdown suppressed cell proliferation and suppressed cell migration and invasion of osteosarcoma cell lines MG-63 and HOS. Functional experiments demonstrated that DIAPH3 knockdown inhibited subcutaneous tumor growth and lung metastasis in vivo. In conclusion, DIAPH3 expression can predict the clinical outcome of osteosarcoma. In addition, DIAPH3 is involved in the proliferation and metastasis of osteosarcoma, and as such, DIAPH3 may be a potential therapeutic target for osteosarcoma.


Aging ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 4141-4151 ◽  
Author(s):  
He Ming ◽  
Qiu Chuang ◽  
Wang Jiashi ◽  
Li Bin ◽  
Wang Guangbin ◽  
...  

Author(s):  
Zhao-Ming Xiao ◽  
Dao-Jun Lv ◽  
Yu-zhong Yu ◽  
Chong Wang ◽  
Tao Xie ◽  
...  

BackgroundSWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin subfamily C member 1 (SMARCC1) protein is a potential tumor suppressor in various cancers. However, its role in prostate cancer (PCa) remains controversial. The aim of this study was to determine the biological function of SMARCC1 in PCa and explore the underlying regulatory mechanisms.MethodsThe expression of SMARCC1 was validated in PCa tissues by immunohistochemistry. Meanwhile, function experiments were used to evaluate the regulatory role on cell proliferation and metastasis in PCa cells with SMARCC1 depletion both in vitro and in vivo. The expression levels of relevant proteins were detected by Western blotting.ResultsOur finding showed that SMARCC1 was significantly downregulated in prostate adenocarcinoma, with a higher Gleason score (GS) than that in low GS. The decreased expression of SMARCC1 was significantly correlated with a higher GS and poor prognosis. Additionally, we found that silencing of SMARCC1 dramatically accelerated cell proliferation by promoting cell cycle progression and enhancing cell migration by inducing epithelial mesenchymal transition (EMT). Furthermore, depletion of SMARCC1 facilitated PCa xenograft growth and lung metastasis in murine models. Mechanistically, the loss of SMARCC1 activated the PI3K/AKT pathway in PCa cells.ConclusionSMARCC1 suppresses PCa cell proliferation and metastasis via the PI3K/AKT signaling pathway and is a novel therapeutic target.


2021 ◽  
Author(s):  
Ruhua Wang ◽  
Yunong Fu ◽  
Menglin Yao ◽  
Xiaomeng Cui ◽  
Yan Zhao ◽  
...  

Abstract Background: The oxaliplatin-based chemotherapy has revealed an encouraging therapeutic efficacy for advanced hepatocellular carcinoma patients. However, the development of resistance limits its clinical utilization. In addition, the chemotherapy resistance in HCC is usually accompanied with other malignant phenotypes, such as cell proliferation and metastasis, which together result in poor prognosis of HCC patients. Therefore, efforts should be made to explore potential regulators which fuel multiple events of HCC progression.Methods: The qRT-PCR, western blot, immunohistochemistry and immunofluorescence were performed to measure mRNA and protein expression. MTT assay, colony formation and Transwell assay were performed to evaluate cell proliferation and metastasis. Flow cytometry was performed to test cell apoptosis. Alkaline Comet assay was performed to measure DNA lesions. Transmission electron microscope analysis provided potent testimony of autophagy. The role of HN1 on the malignant phenotypes of hepatoma carcinoma was demonstrated in vitro and in vivo.Results: The immunohistochemistry analysis of HCC patient tissues revealed that the expression of HN1 was higher in HCC tissues compared to adjacent tissues and was associated with worse prognosis. In vitro, HN1 knockdown inhibited proliferation and metastasis of HCC cells, whereas HN1 overexpression promoted their proliferation and metastasis. In addition, we found that HN1 knockdown sensitized HCC cells to oxaliplatin, which is companied with deteriorated DNA damage and increased cell apoptosis in oxaliplatin-treated HCC cells. In vivo, HN1 knockdown inhibited the tumor growth and metastasis, and promoted the anti-cancer efficiency of oxaliplatin. Mechanically, HN1 prevented HMGB1 from ubiquitination and degradation via autophagy-lysosome pathway, which is related to its interaction with TRIM28, and overexpression of HMGB1 can restore the malignant phenotypes of HN1 knockdown in HCC cells. Furthermore, we found that HN1 can regulate cellular autophagy via HMGB1, which is important to tumor-promoting effect of HN1.Conclusions: In conclusion, we systemically revealed the multiple functions of HN1 in HCC progression and the underlying molecular mechanism, which indicated that HN1 could be a promising therapeutic target for HCC treatment.


Aging ◽  
2018 ◽  
Vol 10 (6) ◽  
pp. 1294-1305 ◽  
Author(s):  
Wang Jiashi ◽  
Qiu Chuang ◽  
Zhang Zhenjun ◽  
Wang Guangbin ◽  
Li Bin ◽  
...  

2021 ◽  
Vol 11 (9) ◽  
pp. 1683-1690
Author(s):  
Yong Duan ◽  
Jin Hai Tan ◽  
Sheng Xiang Tao ◽  
SiYi Liu ◽  
Qian Jin Zheng

The cancerous and matched para-carcinoma tissues were gained from total of 40 patients with OS, miR-30e-5p level was monitored through qRT-PCR, and the relevance between abnormal expressed miR-30e-5p and clinical indicators was uncovered. Simultaneously, miR-30e-5p expressive level in common-applied OS cells was detected by qRT-PCR. Additionally, miR-30e-5p suppression and overexpression models were constructed, and CCK-8 and transwell procedures were subsequently executed to analyze the influences of miR-30e-5p in OS cells. Further, relation between miR-30e-5p and CTHRC1 was forecased, meanwhile CTHRC1 function in miR-30e-5p-modulated OS cells was explored. Low expressed miR-30e-5p is linked to the distant metastasis and poor prognosis, which may restrain the malignant progression of OS by targeting CTHRC1.


2018 ◽  
Vol Volume 12 ◽  
pp. 147-156 ◽  
Author(s):  
Su Hu ◽  
Li Xu ◽  
Lihua Li ◽  
Dongdong Luo ◽  
Hailin Zhao ◽  
...  

2015 ◽  
Vol 35 (4) ◽  
Author(s):  
Qinying Liu ◽  
Yangmei Xu ◽  
Shenghong Wei ◽  
Wei Gao ◽  
Li Chen ◽  
...  

Our study revealed that miR-148b was specifically down-regulated in hepatic cancer stem cells (HCSCs) and affected cell proliferation and metastasis in vitro and tumorigenicity in vivo by directly targeting to Neuropilin-1(NRP-1), a transmembrane co-receptor involved in metastasis, suggesting that enforced miR-148b expression might be an efficient therapeutic strategy to eradicate HCSCs and reduce metastasis.


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