TRIM65 supports bladder urothelial carcinoma cell aggressiveness by promoting ANXA2 ubiquitination and degradation
In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. (Source: Cancer Letters)
Source: Cancer Letters - August 1, 2018 Category: Cancer & Oncology Authors: Wen-Su Wei, Xin Chen, Li-Yi Guo, Xiang-Dong Li, Ming-Hui Deng, Gang- Jun Yuan, Le-Ye He, Yong-Hong Li, Zhi-Lin Zhang, Li-Juan Jiang, Ri-Xin Chen, Xiao-Dan Ma, Shi Wei, Ning-Fang Ma, Zhuo-Wei Liu, Jun-Hang Luo, Fang-Jian Zhou, Dan Xie Tags: Original Articles Source Type: research
Exosomes in cancer: Small transporters with big functions
Exosomes are nanosized membrane-bound vesicles containing abundant proteins, DNA, mRNA, and non-coding RNAs. Exosomes are now considered as an additional mechanism for intercellular communication, allowing cells to exchange proteins, lipids and genetic material. Increasing studies have shown that exosomes play an important role in tumour initiation, growth, progression, metastasis, drug resistance and immune escape. In this article, we review recent advances in the biology of exosomes. We elaborate the specific mechanism by which exosomes affect the communication between tumours and the microenvironment. (Source: Cancer Letters)
Source: Cancer Letters - July 30, 2018 Category: Cancer & Oncology Authors: Xi Li, Yanan Wang, Qi Wang, Yinping Liu, Wei Bao, Sufang Wu Tags: Mini-review Source Type: research
Co-inhibition of BET and proteasome enhances ER stress and Bim-dependent apoptosis with augmented cancer therapeutic efficacy
Agents that inhibit bromodomain and extra-terminal domain (BET) protein have been actively tested in the clinic as potential anticancer drugs. Proteasome inhibitors such as carfilzomib (CFZ) are FDA-approved for the treatment of patients with advanced multiple myeloma and have been tested against other cancers. The current study focuses on the combination of a BET inhibitor (e.g., JQ1) and a proteasome inhibitor (e.g., CFZ) as a novel cancer therapeutic strategy and the underlying mechanisms. The tested combination (JQ1 with CFZ) synergistically decreased cell survival and enhanced apoptosis in vitro and inhibited tumor gr...
Source: Cancer Letters - July 27, 2018 Category: Cancer & Oncology Authors: Guoqing Qian, Weilong Yao, Shuo Zhang, Richa Bajpai, Williams D. Hall, Mala Shanmugam, Sagar Lonial, Shi-Yong Sun Tags: Original Articles Source Type: research
Editorial Board
(Source: Cancer Letters)
Source: Cancer Letters - July 26, 2018 Category: Cancer & Oncology Source Type: research
miR-1273g silences MAGEA3/6 to inhibit human colorectal cancer cell growth via activation of AMPK signaling
AMP-activated protein kinase (AMPK) is a metabolic regulator that acts to limit the growth of cancer cells. AMPK is downregulated by melanoma antigens A3/6 (MAGEA3/6), which are cancer-specific proteins that enhance the activity of specific E3 ubiquitin ligases to ubiquitinate and degrade AMP-activated protein kinase α1 (AMPKα1). Here, using a bioinformatic approach, we identified a microRNA, miR-1273 g-3p, that is predicted to target the 3’ untranslated region (UTR) of MAGEA3/6. Analyzing miR-1273 g-3p expression in human colon cancer tissues, we found a reduction in miR-1273 g-3p expression correlati ng with in...
Source: Cancer Letters - July 26, 2018 Category: Cancer & Oncology Authors: Fang Wu, Fang Liu, Lemei Dong, Han Yang, Xixi He, Lili Li, Lihao Zhao, Sisi Jin, Gang Li Tags: Original Articles Source Type: research
USP10 suppresses tumor progression by inhibiting mTOR activation in hepatocellular carcinoma
Dysregulation of deubiquitination pathway is associated with poor prognosis in cancers such as hepatocellular carcinoma (HCC). The mammalian target of rapamycin, mTOR, has become an attractive cancer therapeutic target in HCC. However, whether and how aberrant expression of deubiquitination pathway regulates mTOR pathway has remained elusive. Here we report that ubiquitin-specific protease 10 (USP10) functions as a tumor suppressor which inhibits mTOR pathway by stabilizing PTEN and AMPK α in HCC cells. (Source: Cancer Letters)
Source: Cancer Letters - July 26, 2018 Category: Cancer & Oncology Authors: Chang Lu, Zhen Ning, Aman Wang, Di Chen, Xiaolong Liu, Tian Xia, Dinesh Singh Tekcham, Wen Wang, Tongming Li, Xiumei Liu, Jing Liu, Huan Qi, Haifeng Luo, Jian Du, Chi Ma, Qiu Yan, Jiwei Liu, Guowang Xu, Hai-long Piao, Guang Tan Tags: Original Articles Source Type: research
Targeting autophagy by small molecule inhibitors of vacuolar protein sorting 34 (Vps34) improves the sensitivity of breast cancer cells to Sunitinib
In this study we systematically screened a library of 306 known anti-cancer drugs for their ability to induce autophagy using a cell-based assay. 114 of the drugs were classified as autophagy inducers; for 16 drugs, the cytotoxicity was potentiated by siRNA-mediated knock-down of Atg7 and Vps34. These drugs were further evaluated in breast cancer cell lines for autophagy induction, and two tyrosine kinase inhibitors, Sunitinib and Erlotinib, were selected for further studies. (Source: Cancer Letters)
Source: Cancer Letters - July 25, 2018 Category: Cancer & Oncology Authors: Matheus Dyczynski, Yasmin Yu, Magdalena Otrocka, Santiago Parpal, Tiago Braga, Aine Brigette Henley, Henric Zazzi, Mikael Lerner, Krister Wennerberg, Jenny Viklund, Jessica Martinsson, Dan Grand ér, Angelo De Milito, Katja Pokrovskaja Tamm Tags: Original Articles Source Type: research
Junctional adhesion molecules mediate transendothelial migration of dendritic cell vaccine in cancer immunotherapy
In vitro generated dendritic cells (DCs) have been studied in cancer immunotherapy for decades. However, the detailed molecular mechanism underlying transendothelial migration (TEM) of DC vaccine across the endothelial barrier to regional lymph nodes (LNs) remains largely unknown. Here, we found that junctional adhesion molecule (JAM)-Like (JAML) is involved in the TEM of mouse bone marrow-derived DCs (BMDCs). Treatment with an anti-JAML antibody or JAML knock-down significantly reduced the TEM activity of BMDCs, leading to impairment of DC-based cancer immunotherapy. (Source: Cancer Letters)
Source: Cancer Letters - July 25, 2018 Category: Cancer & Oncology Authors: Seung-Eon Roh, Yideul Jeong, Myeong-Ho Kang, Yong-Soo Bae Tags: Original Articles Source Type: research
Viewing the Eph Receptors with a focus on Breast Cancer Heterogeneity
Aberrant expression of different family members of the Eph/ephrin system, which comprises the Eph receptors (Ephs) and their ligands (ephrins), has been implicated in various malignancies including breast cancer. The latter presents as a heterogeneous disease with diverse molecular, morphologic and clinical behavior signatures. This review reflects the existing Eph/ephrin literature while focusing on breast cancer heterogeneity. Hormone positive, HER2 positive and triple negative breast cancer (TNBC) cell lines, xenografts/mutant animal models and patient samples are examined separately as, in humans, they represent entiti...
Source: Cancer Letters - July 25, 2018 Category: Cancer & Oncology Authors: Ilias Nikas, Han Suk Ryu, Stamatios Theocharis Tags: Mini-review Source Type: research
Recent findings regarding let-7 in immunity
Let-7 was one of the first microRNAs discovered in Caenorhabditis elegans. It exerts various biological functions, and shows strong evolutionary conservation from nematodes to humans. Recent research findings identify the let-7 cluster as a crucial player in the regulation of B-cell antibody production and macrophage responses. Since increasing evidence supports the let-7 cluster's role in immune system regulation, here we review the latest knowledge regarding the activities of let-7 in both innate and adaptive immune cells —including macrophages, B cells, and subsets of T cells—and the targets regulated by members of ...
Source: Cancer Letters - July 24, 2018 Category: Cancer & Oncology Authors: Shuai Jiang Tags: Mini-review Source Type: research
Reciprocal feedback regulation of ST3GAL1 and GFRA1 signaling in breast cancer cells
GFRA1 and RET are overexpressed in estrogen receptor (ER)-positive breast cancers. Binding of GDNF to GFRA1 triggers RET signaling leading to ER phosphorylation and estrogen-independent transcriptional activation of ER-dependent genes. Both GFRA1 and RET are membrane proteins which are N-glycosylated but no O-linked sialylation site on GFRA1 or RET has been reported. We found GFRA1 to be a substrate of ST3GAL1-mediated O-linked sialylation, which is crucial to GDNF-induced signaling in ER-positive breast cancer cells. (Source: Cancer Letters)
Source: Cancer Letters - July 21, 2018 Category: Cancer & Oncology Authors: Tan-chi Fan, Hui Ling Yeo, Huan-Ming Hsu, Jyh-Cherng Yu, Ming-Yi Ho, Wen-Der Lin, Nai-Chuan Chang, John Yu, Alice L. Yu Tags: Original Articles Source Type: research
Inhibiting Notch1 enhances immunotherapy efficacy in melanoma by preventing Notch1 dependent immune suppressive properties
We have previously shown that Notch1 plays a critical role in modulating melanoma tumor cell growth and survival. Here we show that Notch1 also contributes to an immune-suppressive tumor microenvironment (TME). Notch1 inhibition reduces immune suppressive cells (i.e. MDSCs and Tregs) while allowing the recruitment of functional CD8(+) T cells, leading to a decrease in the Tregs/CD8(+) ratio, a key parameter in assessing positive responses to immune-checkpoint inhibitors. Inhibition of Notch1 improves the antitumor activity of nivolumab and ipilimumab, particularly when given in combination. (Source: Cancer Letters)
Source: Cancer Letters - July 20, 2018 Category: Cancer & Oncology Authors: Hong Qiu, Patrick M. Zmina, Alex Y. Huang, David Askew, Barbara Bedogni Tags: Original Articles Source Type: research
mTORC2 contributes to the metabolic reprogramming in EGFR tyrosine-kinase inhibitor resistant cells in non-small cell lung cancer
Non-small cell lung cancer (NSCLC) patients with activating EGFR mutations are often successfully treated with EGFR tyrosine kinase inhibitor (TKI) such as erlotinib; however, treatment resistance inevitably occurs. Given tumor metabolism of glucose and therapeutic response are intimately linked, we explored the metabolic differences between isogenic erlotinib-sensitive and -resistant NSCLC cell lines. We discovered that the growth of erlotinib-resistant cells is more sensitive to glucose deprivation. (Source: Cancer Letters)
Source: Cancer Letters - July 20, 2018 Category: Cancer & Oncology Authors: Chun-Te Chiang, Alexandra N. Demetriou, Nolan Ung, Niharika Choudhury, Kimya Ghaffarian, Daniel L. Ruderman, Shannon M. Mumenthaler Tags: Original Articles Source Type: research
Angiotensin receptor blockade attenuates cholangiocarcinoma cell growth by inhibiting the oncogenic activity of Yes-associated protein
Cholangiocarcinoma (CCA) is a destructive malignancy with limited responsiveness to conventional chemotherapy. Although angiotensin receptor blockers (ARBs) have gained attention for their potential anticancer activity, little is known about their effects on CCA. The transcriptional co-activator, Yes-associated protein (YAP) is a critical oncogene in several cancers, including CCA. Following recent evidence showing that YAP is regulated by angiotensin II (AT-II), we investigated the effects of an ARB, losartan, on two human CCA cell lines (KKU-M213 and HuCCT-1) with regards to YAP oncogenic regulation. (Source: Cancer Letters)
Source: Cancer Letters - July 19, 2018 Category: Cancer & Oncology Authors: Soichiro Saikawa, Kosuke Kaji, Norihisa Nishimura, Kenichiro Seki, Shinya Sato, Keisuke Nakanishi, Koh Kitagawa, Hideto Kawaratani, Mitsuteru Kitade, Kei Moriya, Tadashi Namisaki, Akira Mitoro, Hitoshi Yoshiji Tags: Original Articles Source Type: research
Genome-wide identification of transcription factors that are critical to non-small cell lung cancer
To systematically unveil transcription factors (TFs) that are critical to lung carcinogenesis, here we conducted a genome-wide lethality screening in non-small cell lung cancer (NSCLC) cells and reported that among the 1530 TFs tested, 21 genes were required for NSCLC cell proliferation and were negatively or positively associated with overall survival (OS) of patients with NSCLC. These included 11 potential tumor suppressing genes (AFF3, AhR, AR, CBFA2T3, CHD4, KANK2, NR3C2, PTEN, PRDM16, RB1, and STK11) and 10 pot ential oncogenic TFs (BARX1, DLX6, ELF3, EN1, ETV1, FOXE1, HOXB7, IRX4, IRX5, and SALL1). (Source: Cancer Letters)
Source: Cancer Letters - July 18, 2018 Category: Cancer & Oncology Authors: Da-Lin Zhang, Li-Wei Qu, Liang Ma, Yong-Chun Zhou, Gui-Zhen Wang, Xin-Chun Zhao, Chen Zhang, Yan-Fei Zhang, Min Wang, Mei-Ying Zhang, Hong Yu, Bei-Bei Sun, San-Hui Gao, Xin Cheng, Ming-Zhou Guo, Yun-Chao Huang, Guang-Biao Zhou Tags: Original Articles Source Type: research
