TBX2 over-expression promotes nasopharyngeal cancer cell proliferation and invasion

Lv, Yan; Si, Meng; Chen, Nannan; Wang, Yongdong; Ma, Xingkai; Yang, Huijun; Xu, Guang–Yin; Wu, Geping; Cao, Cong

doi:10.18632/oncotarget.17084

Cited by 21 publications

(20 citation statements)

References 33 publications

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“…Complete medium (with fetal bovine serum [FBS]) was added to the lower chamber. After 48 h of incubation, cells on the lower surface of the membrane were fixed, stained and then counted in five random fields [37]. Mitomycin (1.5 μg/mL; Sigma-Aldrich) was always added to exclude the influence of cell proliferation.…”

Section: Transwell Assaymentioning

confidence: 99%

WITHDRAWN: Targeting mTORC1/2 with OSI-027 inhibits proliferation and migration of keloid keratinocytes

Liu

Wang

et al. 2018

Oncotarget

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Keloid is a dermal proliferative disorder characterized by the excessive keratinocyte proliferation and migration. mTOR over-activation is involved in the process. Here, we show that both mTOR complex 1 (mTORC1) and mTORC2 were hyper-activated in keloid-derived primary keratinocytes. OSI-027, an mTOR kinase inhibitor, potently inhibited proliferation and migration of keloid keratinocytes. OSI-027 disrupted the assembly of mTORC1 (mTOR-Raptor) and mTORC2 (mTOR-RictormLST8). Further, OSI-027 completely blocked the phosphorylations of the mTORC1 substrates (S6K1, S6 and 4EBP1) and the mTORC2 substrate (AKT, at Ser-473). OSI-027 was potent than rapamycin in inhibiting keloid keratinocytes. Moreover, restoring mTORC1 activation by the introduction of the constitutively active S6K1 only partly alleviated OSI-027-induced suppression on keloid keratinocytes. Notably, mTOR2 inhibition by Rictor siRNA also inhibited keloid keratinocyte proliferation and migration, although less efficiently than OSI-027. Together, concurrent targeting of mTORC1/2 by OSI-027 potently inhibits keloid keratinocyte proliferation and migration.www.impactjournals.com/oncotarget/ Vol.9, (No.1), Supplement 1, pp: s147-s154

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Section: Transwell Assaymentioning

confidence: 99%

WITHDRAWN: Targeting mTORC1/2 with OSI-027 inhibits proliferation and migration of keloid keratinocytes

Liu

Wang

et al. 2018

Oncotarget

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“…It regulates cell cycle progression (Bilican and Goding 2006), and its overexpression has been demonstrated in promoting or maintaining the proliferation of many cancers including melanomas (Vance et al 2005), nasopharyngeal cancer (Lv et al 2017), breast cancer D'Costa et al 2014), prostate cancer (Du et al 2017), and gastric cancer (Yu et al 2015). Here, we show that three copies of the TBX2 gene exist in HepG2 cancer cells as a result of duplication in Haplotype 2.…”

Section: Cc-by-nc-ndmentioning

confidence: 65%

Haplotype-resolved and integrated genome analysis of the cancer cell line HepG2

Zhou

Greer

Spies

et al. 2018

Preprint

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HepG2 is one of the most widely used human cell lines in biomedical research and one of the main cell lines of ENCODE. Although the functional genomic and epigenomic characteristics of HepG2 are extensively studied, its genome sequence has never been comprehensively analyzed and higher-order structural features of its genome beyond its karyotype were only cursorily known. The high degree of aneuploidy in HepG2 renders traditional genome variant analysis methods challenging and partially ineffective. Correct and complete interpretation of the extensive functional genomics data fromHepG2 requires an understanding of the cell line's genome sequence and genome structure. We performed deep whole-genome sequencing, mate-pair sequencing and linked-read sequencing to identify a wide spectrum of genome characteristics in HepG2: copy numbers of chromosomal segments, SNVs and Indels (both corrected for copynumber), phased haplotype blocks, structural variants (SVs) including complex genomic rearrangements, and novel mobile element insertions. A large number of SVs were phased, sequence assembled and experimentally validated. Several chromosomes show striking loss of heterozygosity. We re-analyzed HepG2 RNA-Seq and wholegenome bisulfite sequencing data for allele-specific expression and phased DNA methylation. We show examples where deeper insights into genomic regulatory complexity could be gained by taking knowledge of genomic structural contexts into account. Furthermore, we used the haplotype information to produce an allele-specific CRISPR targeting map. This comprehensive whole-genome analysis serves as a resource for future studies that utilize HepG2.

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“…The detailed protocol of qRT-PCR was described in detail in our previous studies [24-26]. Total RNA was extracted, quantified and reversely-transcribed into complementary DNA via the First-Strand cDNA Synthesis Kit (Thermo Fisher, Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

“…The detailed protocol of IHC staining was described early [24]. In brief, the GC tumor tissues and adjacent normal tissues were fixed in 4% paraform, embedded in paraffin, and cut into 4-μm sections.…”

Section: Methodsmentioning

confidence: 99%

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Overexpression of Lymphocyte Antigen 6 Complex, Locus E in Gastric Cancer Promotes Cancer Cell Growth and Metastasis

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Lymphocyte antigen 6 complex, locus E (LY6E) is a member of the lymphostromal cell membrane Ly6 superfamily protein. The present study investigated the clinical significance and potential biological function of LY6E in gastric cancer (GC). Methods: LY6E mRNA and protein expressions in human GC tissues and GC cells were tested. Relationship between LY6E expression and the GC patients’ clinicopathologic characteristics was analyzed. LY6E was silenced by siRNA in the cultured GC cells. Results: The RNA expression microarray profiling assay results demonstrated that LY6E mRNA was significantly increased in multiple human GC tumor tissues. Immunohistochemistry (IHC) staining analysis revealed that 59 of 75 (78.7%) GC specimens were LY6E positive. LY6E over-expression in human GC was correlated with the histology grade, AJCC stage, N classification, lymphatic invasion, and tumor location. Notably, functional LY6E expression was also detected in AGS and other established GC cell lines. LY6E knockdown by targeted-siRNA inhibited AGS cell survival and proliferation. Meanwhile, the LY6E siRNA induced G1-S cell cycle arrest and apoptosis in AGC cells. Additionally, AGC cell migration was also inhibited by LY6E knockdown. Expressions of tumor-suppressing proteins, including PTEN (phosphatase and tensin homolog) and E-Cadherin, were increased in LY6E-silenced AGS cells. Conclusion: LY6E over-expression in GC is potentially required for cancer cell survival, proliferation and migration.

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TBX2 over-expression promotes nasopharyngeal cancer cell proliferation and invasion

Cited by 21 publications

References 33 publications

WITHDRAWN: Targeting mTORC1/2 with OSI-027 inhibits proliferation and migration of keloid keratinocytes

WITHDRAWN: Targeting mTORC1/2 with OSI-027 inhibits proliferation and migration of keloid keratinocytes

Haplotype-resolved and integrated genome analysis of the cancer cell line HepG2

Overexpression of Lymphocyte Antigen 6 Complex, Locus E in Gastric Cancer Promotes Cancer Cell Growth and Metastasis

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