Evidence map›Paper›PMID 29463274›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Along with its favorable prognostic role, CLCA2 inhibits growth and metastasis of nasopharyngeal carcinoma cells via inhibition of FAK/ERK signaling.

Yuan-Yuan Qiang, Chang-Zhi Li, Rui Sun, Li-Sheng Zheng, Li-Xia Peng, Jun-Ping Yang, Dong-Fang Meng, Yan-Hong Lang, Yan Mei, Ping Xie and 10 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 50 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 5 institutions in 1 country.

Yuan-Yuan QiangState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Chang-Zhi LiState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Rui SunDepartment of Nasopharyngeal Carcinoma, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Li-Sheng ZhengState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Li-Xia PengState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Jun-Ping YangState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Dong-Fang MengState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Yan-Hong LangState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Yan MeiState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Ping XieDepartment of Radiation Oncology, Longyan First Hospital, Affiliated to Fujian Medical University, Longyan, Fujian, China.
Liang XuState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Yun CaoDepartment of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Wen-Wen WeiDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Li CaoDepartment of Pharmacy, Zhongshan People's Hospital, Zhongshan, Guangdong, China.
Hao HuDepartment of Traditional Chinese Medicine, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Qin YangState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Dong-Hua LuoDepartment of Nasopharyngeal Carcinoma, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Ying-Ying LiangDepartment of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China.
Bi-Jun HuangState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Chao-Nan QianState Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China. qianchn@sysucc.org.cn.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNFirst Affiliated Hospital of Fujian Medical University · CNGuangzhou Medical University · CNZhongshan People's Hospital · CN

Funding

National High Technology Research and Development Program of China 2012AA02A501National Natural Science Foundation of China 81272340National Natural Science Foundation of China 81402248National Natural Science Foundation of China 81472386National Natural Science Foundation of China 81502194National Natural Science Foundation of China 81672872Provincial Natural Science Foundation of Guangdong 2016A030311011Science and Technology Planning Project of Guangdong Provinc 2014A020209024Science and Technology Planning Project of Guangdong Province 2014B020212017Science and Technology Planning Project of Guangdong Province 2014B050504004Science and Technology Planning Project of Guangdong Province 2015B050501005
6 · The paper itself

Abstract

backgroundCLCA2 was reported as a tumor suppressor and disregulated in breast cancer. However, its function in tumor growth and metastasis in NPC has rarely been reported. In this study, we investigated the functional and molecular mechanisms by which CLCA2 influences NPC.

methodsCLCA2 expression in human NPC cell lines and tissues was examined via real-time PCR (RT-PCR), Western blot and IHC. The biological roles of CLCA2 in proliferative, migration and invasion of NPC cell lines was evaluated in 5-8F, S18, S26 and SUNE-1 cells. Cell viability, migration and invasion were assessed in vitro by MTS, colony formation and transwell assay, respectively. CLCA2 in growth and metastasis of NPC were evaluated in vivo through NPC xenograft tumor growth, lung metastatic mice model and popliteal lymph node (LN) metastasis model.

resultsOverexpression of CLCA2 significantly decreased proliferation, migration and invasion of NPC cells. In contrast, knockdown of CLCA2 elicited the opposite effects. CLCA2 overexpression suppressed xenograft tumor growth and lung, popliteal lymph node (LN) metastasis in vivo. CLCA2 inhibited tumor metastasis through suppressing epithelial-Mesenchymal transition (EMT) and in-activating FAK/ERK1/2 signaling pathway in NPC cells. Immunohistochemical staining of 143 NPC samples revealed that CLCA2 expression was an independent, favorable prognostic factor for overall survival and distant metastasis-free survival of patients. In addition, inhibition of FAK and ERK1/2 reversed CLCA2 silencing-induced tumor cell migration. Furthermore, inhibitors against chloride channels suppressed NPC cellular migration which could have been enhanced by the presence of CLCA2.

conclusionCLCA2 suppress NPC proliferation, migration, invasion and epithelial-mesenchymal transition through inhibiting FAK/ERK signaling.

Indexed as

AdultAgedAnimalsCell Line, TumorCell MovementCell SurvivalChloride ChannelsDisease Models, AnimalEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesFemaleFocal Adhesion Kinase 1Gene ExpressionHumansMaleMiceChloride ChannelsCLCA2 protein, humanExtracellular Signal-Regulated MAP KinasesFocal Adhesion Kinase 1PTK2 protein, humanCLCA2FAK/ERKMetastasisNasopharyngeal carcinomaPrognostics

Identifiers

PMID29463274
PMCPMC5819171
OpenAlexW2793298349

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.