Up-regulation of OLR1 expression by TBC1D3 through activation of TNFα/NF-κB pathway promotes the migration of human breast cancer cells

Wang, Bei; Zhao, Hai Tao; Zhao, Lei; Zhang, Yongchen; Wan, Qing; Shen, Yong; Bu, Xiaodong; Wan, Meiling; Shen, Chuanlu

doi:10.1016/j.canlet.2017.08.021

Cited by 41 publications

(29 citation statements)

References 54 publications

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“…To enable the thorough exploration of LINC00467 in the molecular regulation of HCC, the UCSC database was utilized and then the gene for TRAF5 was discovered to be a neighboring gene of that for LINC00467. As a result of the significant role of TRAF5 in the progression of different cancers, such as colorectal cancer, prostate cancer and breast cancer, TRAF5 was selected to be studied. In the present study, the expression of TRAF5 was positively modulated by LINC00467 in HCC.…”

Section: Discussionmentioning

confidence: 99%

LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinoma

Jiang

Cheng

Wang

et al. 2020

The Journal of Gene Medicine

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Background Hepatocellular carcinoma (HCC) has been recognized as a member of the most common human malignant tumors globally. According to multiple studies, long noncoding RNAs (lncRNAs) have been defined as vital regulators in tumor progression. Although previous studies have indicated that lncRNA long intergenic non‐protein coding RNA 467 (LINC00467) exerts oncogenic effect in tumorigenesis and the development of cancers, the specific function that LINC00467 induces in HCC remains obscure. Methods LINC00467 expression was examined by a quantitative reverse transcriptase‐polymerase chain reaction. CCK‐8, EdU, transwell, western blotting and caspase‐3 activity analyses were utilized to testify the role of LINC00467 in HCC. The interaction between IGF2BP3 and LINC00467 (or TRAF5) was investigated by luciferase reporter, RIP and RNA pull‐down assays. Results LINC00467 upregulation in HCC tissues and cells was observed. LINC00467 silencing suppressed cell proliferation and metastasis, whereas it facilitated cell apoptosis in HCC. The gene for tumor necrosis factor receptor‐associated factor 5 (TRAF5) was a neighboring gene of that for LINC00467 and its expression was positively modulated by LINC00467 in HCC. TRAF5 knockdown inhibited HCC progression. LINC00467 deficiency could decrease the mRNA stability of TRAF5 in HCC. Insulin‐like growth factor‐2 messenger RNA‐binding protein 3 (IGF2BP3) could bind with LINC00467 and its depletion could lower TRAF5 mRNA stability in HCC. Final rescue assays further indicated that downregulation of IGF2BP3 or TRAF5 acted against LINC00467 upregulation‐mediated function on HCC progression. Conclusions LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in HCC.

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Section: Discussionmentioning

confidence: 99%

LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinoma

Jiang

Cheng

Wang

et al. 2020

The Journal of Gene Medicine

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“…Based on online literature search, we found that OLR1, GPNMB, PRRX1 and BCAT1 promote cancer migration and invasion in various types of cancer. Specifically, OLR1 has been recognized as a cell migration stimulator in breast cancer cells, and potentially up‐regulated by oncogene TBC1D3 through activation of TNFa/NF‐ K B pathway . Non‐metastatic glycoprotein melanoma protein B (GPNMB), also known as osteoactivin (OA) is expressed in verified tumours and represents an emerging target for drug development.…”

Section: Discussionmentioning

confidence: 99%

In vitro and clinical data analysis of Osteopontin as a prognostic indicator in colorectal cancer

Wei

Wong

Lyu

et al. 2018

J Cellular Molecular Medi

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Osteopontin (OPN) has been shown to promote colorectal cancer (CRC) progression; however, the mechanism of OPN‐induced CRC progression is largely unknown. In this study, we found that OPN overexpression led to enhanced anchorage‐independent growth, cell migration and invasion in KRAS gene mutant cells but to a lesser extent in KRAS wild‐type cells. OPN overexpression also induced PI3K signalling, expression of Snail and Matrix metallopeptidase 9 (MMP9), and suppressed the expression of E‐cadherin in KRAS mutant cells. In human CRC specimens, a high‐level expression of OPN significantly predicted poorer survival in CRC patients and OPN expression was positively correlated with MMP9 expression, and negatively correlated with E‐cadherin expression. Furthermore, we have found that 15 genes were co‐upregulated in OPN highly expression CRC and a list of candidate drugs that may have potential to reverse the secreted phosphoprotein 1 (SPP1) gene signature by connectivity mapping. In summary, OPN is a potential prognostic indicator and therapeutic target for colon cancer.

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“…Their results showed that this factor was highly expressed in MDA-MB-231 cells; furthermore, a downregulation of CD74 inhibited both migration and invasion of MDA-MB-231 cells. Wang et al [ 88 ] reported that TBC1D3 oncogene promotes the migration of breast cancer cells, and its interaction with calmodulin enhances the effects of TBC1D3.…”

Section: Discussionmentioning

confidence: 99%

Migration Rate Inhibition of Breast Cancer Cells Treated by Caffeic Acid and Caffeic Acid Phenethyl Ester: An In Vitro Comparison Study

et al. 2017

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One of the deadliest cancers among women is a breast cancer. Research has shown that two natural substances occurring in propolis, caffeic acid (CA) and caffeic acid phenethyl ester (CAPE), have significant anticancer effects. The purpose of our in vitro study was to compare cytotoxic activity and migration rate inhibition using CA and CAPE (doses of 50 and 100 µm) against triple-negative, MDA-MB-231 breast adenocarcinoma line cells, drawn from Caucasian women. Viability was measured by XTT-NR-SRB assay (Tetrazolium hydroxide-Neutral Red-Sulforhodamine B) for 24 h and 48 h periods. Cell migration for wound healing assay was taken for 0 h, 8 h, 16 h, and 24 h periods. CAPE displayed more than two times higher cytotoxicity against MDA-MB-231 cells. IC50 values for the XTT assay were as follows: CA for 24 h and 48 h were 150.94 µM and 108.42 µM, respectively, while CAPE was 68.82 µM for 24 h and 55.79 µM for 48 h. For the NR assay: CA was 135.85 µM at 24 h and 103.23 µM at 48 h, while CAPE was 64.04 µM at 24 h and 53.25 µM at 48 h. For the SRB assay: CA at 24 h was 139.80 µM and at 48 h 103.98 µM, while CAPE was 66.86 µM at 24 h and 47.73 µM at 48 h. Both agents suspended the migration rate; however, CAPE displayed better activity. Notably, for the 100 µM CAPE dose, motility of the tested breast carcinoma cells was halted.

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Up-regulation of OLR1 expression by TBC1D3 through activation of TNFα/NF-κB pathway promotes the migration of human breast cancer cells

Cited by 41 publications

References 54 publications

LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinoma

LINC00467 promotes cell proliferation and metastasis by binding with IGF2BP3 to enhance the mRNA stability of TRAF5 in hepatocellular carcinoma

In vitro and clinical data analysis of Osteopontin as a prognostic indicator in colorectal cancer

Migration Rate Inhibition of Breast Cancer Cells Treated by Caffeic Acid and Caffeic Acid Phenethyl Ester: An In Vitro Comparison Study

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