Dongling Zou^*, Qi Zhou^†, Dong Wang^†, Lili Guan^*, Li Yuan^*†, Shaolin Li^*

Oncology Research, Vol.24, No.2, pp. 99-108, 2016, DOI:10.3727/096504016X14611963142173

Abstract It has been demonstrated that microRNAs (miRNAs) act as oncogenes or tumor suppressors in a variety of cancers. Our previous work suggested that miR-10a/b functioned as a tumor suppressor in gastric cancer, and miR-10b was also reported to be significantly downregulated in advanced stage cervical cancer tissues. However, the aberrant expression of miR-10b in cervical cancer and its possible role in cervical carcinogenesis was largely unknown. In this study, we investigated the expression of miR-10b in cervical cancer tissues, carcinoma in situ tissues, mild dysplasia, moderate dysplasia, severe dysplasia tissues, and normal controls. We found More >

Ye Lou^*1, Lei Liu^†1, Lihui Zhan^‡, Xuewei Wang^§, Hua Fan^¶

Oncology Research, Vol.24, No.2, pp. 89-97, 2016, DOI:10.3727/096504016X14597766487753

Abstract Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy and causes a high rate of mortality in affected adults. Many subtypes of ALL exist with disruptions in distinct genetic pathways, including those regulated by miRNAs. Here we identify miR-187-5p as being highly upregulated in B-cell ALL and a driver of cellular proliferation and suppressor of apoptosis. We show that miR-187-5p directly targets the 3'-UTR of DKK2 to mediate these effects. We further determine that inhibition of DKK2 by miR-187-5p in Nalm-6 B cells leads to inappropriate activation of Wnt/β-catenin signaling. Together, these findings reveal More >

Shenggang Liu^*, Hongzhong Yang^†, Ying Chen^‡, Baimei He^§, Qiong Chen^§

Oncology Research, Vol.24, No.2, pp. 81-87, 2016, DOI:10.3727/096504016X14597766487717

Abstract In order to improve therapeutic efficacy, it is a current emergency to better know the mechanisms underlying cisplatin resistance in lung cancer cells. In this study, we aim to investigate the role of Krüppel-like factor 4 (KLF4) in cisplatin-resistant lung cancer cells. We developed cisplatin-resistant lung cancer cell line A549/ DDP, and then a battery of experiments was used to analyze the effects of KLF4 in cisplatin resistance of lung cancer. We found that KLF4 was significantly downregulated in cisplatin-resistant A549 cells and forced KLF4 expression inhibited cell growth and induced apoptosis. Further, we found More >

Annie Im, Ali Amjad, Mounzer Agha, Anastasios Raptis, Jing-Zhou Hou, Rafic Farah, Seah Lim, Alison Sehgal, Kathleen A. Dorritie, Robert L. Redner, Brian McLaughlin, Yongli Shuai, Shrina Duggal, Michael Boyiadzis

Oncology Research, Vol.24, No.2, pp. 73-80, 2016, DOI:10.3727/096504016X14586627440156

Abstract Relapsed acute myeloid leukemia (AML) represents a major therapeutic challenge. Achieving complete remission (CR) with salvage chemotherapy is the first goal of therapy for relapsed AML. However, there is no standard salvage chemotherapy. The current study evaluated outcomes and prognostic factors for achievement of CR in 91 AML patients in first relapse who were treated with the mitoxantrone–etoposide combination regimen. The overall response rate (CR and CRi) was 25%. Factors that were associated with a lower rate of CR included older age, shorter duration of first CR, low hemoglobin, and low platelet count. The median… More >

Pei Yin^*1, Jinpeng Jia^†1, Jijun Li^*, Yan Song^*, Yiyan Zhang^*, Fengkun Chen^*

Oncology Research, Vol.24, No.1, pp. 65-72, 2016, DOI:10.3727/096504016X14587366983838

Abstract Renal cell carcinoma (RCC) is the most common malignancy in the kidney in the world, and the 5-year overall survival for patients remains poor due to the lack of effective treatment strategies. Although ABT-737, as a Bcl-2/Bcl-xL inhibitor, has recently emerged as a novel cancer therapeutic reagent, apoptosis induced by ABT-737 is often blocked in several types of cancer cells. This study investigated whether the combination of the small-molecule BH3 mimetic ABT-737 and the lysosome inhibitor chloroquine was an effective strategy for treating renal cancer cells. We found that the combination of ABT-737 and chloroquine… More >

Arya Sobhakumari^*1, Kevin P. Orcutt^†‡1, Laurie Love-Homan^§, Christopher E. Kowalski^†‡, Arlene D. Parsons^†, C. Michael Knudson^†‡§¶, Andrean L. Simons^*†‡§¶

Oncology Research, Vol.24, No.1, pp. 55-64, 2016, DOI:10.3727/096504016X14586627440192

Abstract Poor tumor response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is a significant challenge for effective treatment of head and neck squamous cell carcinoma (HNSCC). Therefore, strategies that may increase tumor response to EGFR TKIs are warranted in order to improve HNSCC patient treatment and overall survival. HNSCC tumors are highly glycolytic, and increased EGFR signaling has been found to promote glucose metabolism through various mechanisms. We have previously shown that inhibition of glycolysis with 2-deoxy-d-glucose (2DG) significantly enhanced the antitumor effects of cisplatin and radiation, which are commonly used to treat… More >

Yasemin Baskin^*†‡, Gizem Calibasi Kocal^‡§, Betul Bolat Kucukzeybek^¶, Mahdi Akbarpour^#, Nurcin Kayacik^**, Ozgul Sagol^††, Hulya Ellidokuz^†‡‡, Ilhan Oztop^§§

Oncology Research, Vol.24, No.1, pp. 41-53, 2016, DOI:10.3727/096504016X14576297492418

Abstract Most of the gastrointestinal stromal tumors (GISTs) have gain-of-function mutations in the KIT gene, which can be used as a prognostic marker for the biological behavior of tumors, predictive marker for the response of tyrosine kinase inhibitors, and diagnostic marker. Researchers have focused on PDGFRA mutations because of both their prognostic and predictive potential and DOG1 positivity for diagnosis on GISTs. The aim of this study is to investigate the effect DOG1, PDGFRA, and KIT mutations on the prediction of the outcome for GIST management. Polymerase chain reaction was performed for KIT gene exons 9, 11, 13,… More >

Guo-ying Zhang¹, Ai-hua Liu¹, Guo-min Li, Jian-rong Wang

Oncology Research, Vol.24, No.1, pp. 33-39, 2016, DOI:10.3727/096504016X14575597858654

Abstract Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP/PBXIP1) is a nucleocytoplasmic shuttling protein, and its expression is associated with cancer aggressiveness. However, the role of HPIP in ovarian cancer is still unclear. Here, we aimed to clarify the role of HPIP in epithelial–mesenchymal transition (EMT) process of ovarian cancer cells, stimulated by transforming growth factor (TGF)-β1. In this study, we found that HPIP was highly expressed in ovarian cancer cells, and TGF-β1 treatment induced HPIP expression in ovarian cancer cells. In addition, knockdown of HPIP suppressed TGF-β1-induced EMT and migration/invasion in ovarian cancer cells. Moreover, More >

Ping He^*, Hong-xia Zhang^†, Chang-yu Sun^*, Chun-yong Chen^‡, He-qing Jiang^*

Oncology Research, Vol.24, No.1, pp. 25-32, 2016, DOI:10.3727/096504016X14575597858609

Abstract The SASH1 (SAM- and SH3-domain containing 1) gene, a member of the SLY (SH3 domain containing expressed in lymphocytes) family of signal adapter proteins, has been implicated in tumorigenesis of many types of cancers. However, the role and mechanism of SASH1 in the invasion and metastasis of hepatocarcinoma are largely unknown. In this study, we investigated the role and mechanism of SASH1 in the invasion and metastasis of hepatocarcinoma. Our results showed that SASH1 was lowly expressed in hepatocarcinoma cell lines. The in vitro experiments showed that overexpression of SASH1 inhibited the proliferation and migration/invasion More >

Wei Zong^*, Chen Yu^†, Ping Wang^*, Lei Dong^‡

Oncology Research, Vol.24, No.1, pp. 17-23, 2016, DOI:10.3727/096504016X14570992647203

Abstract The epithelial–mesenchymal transition (EMT) is considered to be one of the critical steps in gastric cancer cell invasion and metastasis. SAM- and SH3-domain containing 1 (SASH1), a member of the SLY family of signal adapter proteins, is a candidate for tumor suppression in several cancers. However, the biological role of SASH1 in gastric cancer remains largely unknown. Therefore, the purpose of this study was to investigate the impact of SASH1 on the biological behavior of gastric cancer cells treated with transforming growth factor (TGF)-β1. In the current study, we provide evidence that SASH1 was lowly More >