Chang Li^*, Xiaoping Li^†, Shuohui Gao^*, Chang Li^‡, Lianjun Ma^§

Oncology Research, Vol.28, No.7-8, pp. 819-822, 2020, DOI:10.3727/096504021X16240202940003

Abstract Gastric cancer is the fourth most common type of cancer and the second highest leading cause of cancer-related deaths worldwide. It has already been established that miR-133a is involved in gastric cancer. In this study, we investigated the molecular mechanisms by which miR-133a inhibits the proliferation of gastric cancer cells. We analyzed the proliferative capacity of human gastric cancer cells SNU-1 using an MTT assay. Cell apoptosis was determined using flow cytometry. The expression levels of ERBB2, p-ERK1/2, and p-AKT in SNU-1 cells were determined using Western blot analysis. To confirm that ERBB2 is a… More >

Yinghua Li^*†, Songyi Li^†, Lili Huang^*

Oncology Research, Vol.26, No.1, pp. 123-130, 2018, DOI:10.3727/096504017X14912172235777

Abstract Rap2B, belonging to the Ras superfamily, has been implicated in cancer development and functions as a tumor promoter. However, the role of Rap2B in cervical cancer is unknown. In this study, we investigated the expression pattern and biological functions of Rap2B in cervical cancer. The results showed that Rap2B was overexpressed in cervical cancer tissues and cell lines. Knockdown of Rap2B inhibited the proliferation, migration, and invasion of cervical cancer cells. In addition, our tumorigenesis assay showed that Rap2B knockdown suppressed cervical cancer cell growth and metastasis in vivo. We also found that the ERK1/2 More >

Ling Liu, Nianfeng Li, Qi Zhang, Jixiang Zhou, Ling Lin, Xinxin He

Oncology Research, Vol.25, No.9, pp. 1607-1616, 2017, DOI:10.3727/096504017X14938093512742

Abstract Transforming growth factor-b (TGF-β) and ERK signaling have been implicated in various human cancers including hepatocellular carcinoma, but the underlying mechanism remains largely unclear. In this study, we aimed to explore the role of ERK1/2 in the regulation of TGF-β’s promoting and suppressive activities in HCC cells. Our data showed that treatment with TGF-β1 enhanced invasion and epithelial–mesenchymal transition (EMT) in HCC HepG2 cells, accompanied with increased MMP9 production and activation of Smad2/3 and ERK1/2, but inhibited tumor cell proliferation. These effects were eliminated by treatment with SB431542, a TGF-β inhibitor. Afterward, treatment with the… More >

Maitham A. Khajah, Princy M. Mathew, Yunus A. Luqmani

Oncology Research, Vol.25, No.8, pp. 1283-1295, 2017, DOI:10.3727/096504017X14883245308282

Abstract Current mainstream pharmacological options for the treatment of endocrine-resistant breast cancer have limitations in terms of their side effect profile and lack of discrimination between normal and cancer cells. In the current study, we assessed the responses of normal breast epithelial cells MCF10A, estrogen receptorpositive (ER+ ) MCF-7, and ER-silenced pII breast cancer cells to inhibitors (either individually or in combination) of downstream signaling molecules. The expression/activity of ERK1/2, p38 MAPK, and Akt was determined by Western blotting. Cell proliferation, motility, and invasion were determined using MTT, wound healing, and Matrigel assays, respectively. Morphological changes… More >

Chang Li^*, Xiaoping Li^†, Shuohui Gao^*, Chang Li^‡, Lianjun Ma^§

Oncology Research, Vol.25, No.7, pp. 1169-1176, 2017, DOI:10.3727/096504017X14847395834985

Abstract Gastric cancer is the fourth most common type of cancer and the second highest leading cause of cancer-related deaths worldwide. It has already been established that miR-133a is involved in gastric cancer. In this study, we investigated the molecular mechanisms by which miR-133a inhibits the proliferation of gastric cancer cells. We analyzed the proliferative capacity of human gastric cancer cells SNU-1 using an MTT assay. Cell apoptosis was determined using flow cytometry. The expression levels of ERBB2, p-ERK1/2, and p-AKT in SNU-1 cells were determined using Western blot analysis. To confirm that ERBB2 is a… More >

Yaqiong Tian^*1, Zengli Zhang^†1, Liyun Miao^*, Zhimin Yang^‡, Jie Yang^*, Yinhua Wang^§, Danwen Qian^¶, Hourong Cai^*, Yongsheng Wang^*

Oncology Research, Vol.24, No.5, pp. 295-303, 2016, DOI:10.3727/096504016X14648701447814

Abstract Recently, epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have revolutionized nonsmall cell lung cancer (NSCLC) treatment. However, resistance remains a major obstacle. Anexelekto (AXL) is a member of receptor tyrosine kinases (RTKs) and shares the same downstream signaling pathways with EGFR, such as PI3K/AKT and MAPK/ERK. AXL overexpression in resistant tumors has been implicated in many previous studies in vitro and in vivo. In this study, we further examined whether expression of AXL and its downstream targets increased in gefitinib-resistant PC9 cells (PC9GR). In addition, we hypothesize that knocking down AXL in PC9GR and… More >

Sheng Li, Zhengli Cui, Xianfeng Meng

Oncology Research, Vol.24, No.4, pp. 279-286, 2016, DOI:10.3727/096504016X14666990347554

Abstract Poly(ADP-ribose) polymerase 1 (PARP-1) is reported to be involved in DNA repair and is now recognized as a key regulator in carcinogenesis. However, the potential role and the molecular mechanism underlying the effect of PARP-1 on osteosarcoma (OS) cells have not been elucidated. In this study, the results showed that knockdown of PARP-1 resulted in decreased cell proliferation, increased cell apoptosis, and G₀/G₁ phase arrest in U2OS cells. In addition, increased expression of active caspase 3 and Bax, but reduced Bcl-2, cyclin D1, and phosphorylated extracellular signal regulated kinase 1/2 (pERK1/2) were observed in PARP-1 knockdown More >