Transcription factor Sp1 regulates expression of cancer‐associated molecule CD147 in human lung cancer

Kong, Ling‐Min; Liao, Cheng-Gong; Fei, Fei; Guo, Xu; Xing, Jinliang; Chen, Zhinan

doi:10.1111/j.1349-7006.2010.01554.x

Cited by 94 publications

(75 citation statements)

References 28 publications

(36 reference statements)

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“…Western blotting was performed as described previously (22,23). Anti-CD147 mAb was prepared by our laboratory (7).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…The miRNA mimics, antisense miR-22 (As-miR-22), and negative control were synthesized by Genepharma. Cell transfection and dual luciferase reporter assay were performed as described previously (22,23).…”

Section: Real-time Quantitative Rt-pcrmentioning

confidence: 99%

“…Our previous studies reported that transcription factor Sp1 could regulate CD147 expression in lung and liver cancers (22,23). Recently, Sp1 was identified as a direct miR-22 target involved in the cancer cell senescence program (20).…”

Section: Introductionmentioning

confidence: 99%

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A Regulatory Loop Involving miR-22, Sp1, and c-Myc Modulates CD147 Expression in Breast Cancer Invasion and Metastasis

et al. 2014

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Breast cancer is the most common cancer in women for which the metastatic process is still poorly understood. CD147 is upregulated in breast cancer and has been associated with tumor progression, but little is known about its regulatory mechanisms. In this study, we demonstrated that CD147 was overexpressed in breast cancer tissues and cell lines, and the high expression correlated with tumor invasion and metastasis. We also found that the transcription factors Sp1 and c-Myc could bind to the CD147 promoter and enhance its expression. The CD147 mRNA has a 748-bp 3 0 -untranslated region (UTR) with many miRNA target sites, suggesting possible regulation by miRNAs. We discovered that miR-22 repressed CD147 expression by directly targeting the CD147 3 0 UTR. We also determined that miR-22 could indirectly participate in CD147 modulation by downregulating Sp1 expression. miR-22 could form an autoregulatory loop with Sp1, which repressed miR-22 transcription by binding to the miR-22 promoter. Together with the c-Myc-mediated inhibition of miR-22 expression, our investigation identified a miR-22/Sp1/c-Myc network that regulates CD147 gene transcription. In addition, miR-22 overexpression suppressed breast cancer cell invasion, metastasis, and proliferation by targeting CD147 in vitro and in vivo. Furthermore, we found that miR-22 was significantly downregulated in breast cancer tissues and that its expression was inversely correlated with the tumor-node-metastasis stage and lymphatic metastasis in patients. Our study provides the first evidence that an miR-22/Sp1/c-Myc network regulates CD147 upregulation in breast cancer and that miR-22 represses breast cancer invasive and metastatic capacities. Cancer Res; 74(14); 3764-78. Ó2014 AACR.

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“…Western blotting was performed as described previously (22,23). Anti-CD147 mAb was prepared by our laboratory (7).…”

Section: Western Blot Analysismentioning

confidence: 99%

Section: Real-time Quantitative Rt-pcrmentioning

confidence: 99%

See 1 more Smart Citation

A Regulatory Loop Involving miR-22, Sp1, and c-Myc Modulates CD147 Expression in Breast Cancer Invasion and Metastasis

et al. 2014

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“…Aberrant expression of miRNAs has been found to be associated with the development and progression of numerous types of cancers. Existing research shows that aberrant expression of miRNAs has prognostic significance for certain types of cancer, such as lung and esophageal cancer, lymphocytic leukemia and neuroblastoma (13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

miR-125a-5p upregulation suppresses the proliferation and induces the cell apoptosis of lung adenocarcinoma by targeting NEDD9

Zheng

Shi

et al. 2017

Oncology Reports

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Abstract. MicroRNAs (miRNAs) are critical translational regulators that act as oncogenes or tumor-suppressor genes. qRT-PCR assay results showed that the expression levels of miR-125a-5p are lower in lung adenocarcinoma (AD) tissues than expression levels in adjacent non-neoplastic tissues. This relative expression was found to be significantly associated with lymph node metastases. Cell growth, apoptosis, caspase activity and Transwell invasion assay results showed that in two lung adenocarcinoma cell lines transfected with a miR-125a-5p mimic, proliferation and invasion rates were found to be significantly reduced, whereas the apoptosis rate of the miR-125a-5p mimic group was enhanced. Subsequent western blotting and luciferase reporter assays showed that miR-125a-5p is able to bind to putative binding sites within the mRNA 3' untranslated region (UTR) of neural precursor cell expressed, developmentally downregulated 9 (NEDD9). Our findings suggest that miR-125a-5p may serve as a therapeutic agent for lung adenocarcinoma through its major target, NEDD9.

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“…[25][26][27] Sp1 was a eukaryotic transcriptional activator identified and involved in many physiological and pathological processes by regulating gene expression, which is affected by the rate of Sp1 protein synthesis, nuclear translocation, and DNAbinding affinity. 28 Kong et al 29 reported that the expression of Sp1 directly regulated the expression level of CD147 in lung cancer cells. In addition, CD147 promoted Sp1 phosphorylation through the PI3K/AKT and MAPK/ERK pathways.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B X-interacting protein promotes cisplatin resistance and regulates CD147 via Sp1 in ovarian cancer

Zou

Yang

et al. 2017

Exp Biol Med (Maywood)

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We found that hepatitis B X-interacting protein (HBXIP) was able to activate the CD147 promoter through Sp1. In vivo, depletion of HBXIP decreased the tumor volume and weight induced by CP. Taken together, these results indicate that HBXIP promotes cisplatin resistance and regulated CD147 via Sp1 in ovarian cancer cell lines. AbstractOvarian cancer is the highest mortality rate of all female reproductive malignancies. Drug resistance is a major cause of treatment failure in malignant tumors. Hepatitis B X-interacting protein acts as an oncoprotein, regulates cell proliferation, and migration in breast cancer. We aimed to investigate the effects and mechanisms of hepatitis B X-interacting protein on resistance to cisplatin in human ovarian cancer cell lines. The mRNA and protein levels of hepatitis B X-interacting protein were detected using RT-PCR and Western blotting in cisplatin-resistant and cisplatin-sensitive tissues, cisplatin-resistant cell lines A2780/CP and SKOV3/CP, and cisplatin-sensitive cell lines A2780 and SKOV3. Cell viability and apoptosis were measured to evaluate cellular sensitivity to cisplatin in A2780/CP cells. Luciferase reporter gene assay was used to determine the relationship between hepatitis B X-interacting protein and CD147. The in vivo function of hepatitis B X-interacting protein on tumor burden was assessed in cisplatin-resistant xenograft models. The results showed that hepatitis B X-interacting protein was highly expressed in ovarian cancer of cisplatin-resistant tissues and cells. Notably, knockdown of hepatitis B X-interacting protein significantly reduced cell viability in A2780/CP compared with cisplatin treatment alone. Hepatitis B X-interacting protein and cisplatin cooperated to induce apoptosis and increase the expression of c-caspase 3 as well as the Bax/Bcl-2 ratio. We confirmed that hepatitis B X-interacting protein up-regulated CD147 at the protein expression and transcriptional levels. Moreover, we found that hepatitis B X-interacting protein was able to activate the CD147 promoter through Sp1. In vivo, depletion of hepatitis B X-interacting protein decreased the tumor volume and weight induced by cisplatin. Taken together, these results indicate that hepatitis B X-interacting protein promotes cisplatin resistance and regulated CD147 via Sp1 in ovarian cancer cell lines.

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Transcription factor Sp1 regulates expression of cancer‐associated molecule CD147 in human lung cancer

Cited by 94 publications

References 28 publications

A Regulatory Loop Involving miR-22, Sp1, and c-Myc Modulates CD147 Expression in Breast Cancer Invasion and Metastasis

A Regulatory Loop Involving miR-22, Sp1, and c-Myc Modulates CD147 Expression in Breast Cancer Invasion and Metastasis

miR-125a-5p upregulation suppresses the proliferation and induces the cell apoptosis of lung adenocarcinoma by targeting NEDD9

Hepatitis B X-interacting protein promotes cisplatin resistance and regulates CD147 via Sp1 in ovarian cancer

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