Silencing of Livin inhibits tumorigenesis and metastasis via VEGF and MMPs pathway in lung cancer

Lin, Xian; Li, Hongru; Lin, Xiao; Yu, Mei-E; Tu, Xunwei; Hua, Zhi-Dan; Lin, Ming Tsan; Xu, Nengluan; Han, Lili; Chen, Yu‐Sheng

doi:10.3892/ijo.2015.3058

Cited by 22 publications

(16 citation statements)

References 39 publications

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“…(Salajegheh et al 2011, Das & Wakelee 2012, Rajabi et al 2012. In this pathway of tumour angiogenesis and in the downstream of VEGF, many proteins such as MMP2 and MMP9 have been reported to be involved in the enhancement and expansion of neo-angiogenesis process in different malignant lesions (Turner et al 2003, Lin et al 2015, Mahecha & Wang 2017. Interaction of VEGF and MMPs have been reported in lung cancer, endometrial cancer and breast cancer (Radisky & Radisky 2010, Lin et al 2015, Mahecha & Wang 2017.…”

Section: Discussionmentioning

confidence: 99%

miR-205 targets angiogenesis and EMT concurrently in anaplastic thyroid carcinoma

Vosgha¹,

Ariana²,

Smith³

et al. 2018

Endocrine-Related Cancer

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The current study aims to evaluate for the first time the inhibitory roles of in the pathogenesis of anaplastic thyroid carcinoma. In addition, we investigated the mechanisms by which miR-205 regulates angiogenesis and epithelial-to-mesenchymal transition (EMT) in cancer. Two anaplastic thyroid carcinoma cell lines were transfected with the expression vector pCMV- Selected markers of angiogenesis and EMT including vascular endothelial growth factor A () and zinc finger E-box-binding homeobox 1 () were investigated by Western blot. The interaction of expression with EMT and angiogenesis were also investigated by assessment of matrix metalloproteinases 2 and 9 (MMP2 and MMP 9), SNAI1 (Snai1 family zinc finger 1), vimentin, E-cadherin and N-cadherin. The function of was further tested with VEGF enzyme-linked immunosorbent assay (ELISA), wound healing, invasion and tube formation assays. Using an animal model, we studied the association of with angiogenesis, proliferation and invasion. The following results were obtained. Permanent overexpression of significantly suppressed angiogenesis and EMT by simultaneously targeting , and downstream products. Ectopic expression of in cancer cells led to decreased migration, invasion and tube formation of endothelial cells. In addition, inhibition of tumour growth, vascularisation and invasion were noted in the mouse tumour xenografts. Our findings provide insights into simultaneous regulatory role of in the pathogenesis of anaplastic thyroid carcinoma by suppressing both angiogenesis and EMT. This may open avenues to exploit as an alternative cancer therapeutic strategy in the future.

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Section: Discussionmentioning

confidence: 99%

miR-205 targets angiogenesis and EMT concurrently in anaplastic thyroid carcinoma

Vosgha¹,

Ariana²,

Smith³

et al. 2018

Endocrine-Related Cancer

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“…The anti-apoptotic potential of Livin and its preferential expression in osteosarcoma, at very low or undetectable levels in the corresponding normal tissue, suggest that the manipulation of Livin expression could represent a novel and tumor-specific molecular target for cancer therapy (23). Zhuang et al (24) demonstrated that long-term silencing of Livin expression inhibited the proliferation of Livin-expressing non small-cell lung cancer cells and increased the chemosensitivity of NSCLC cells.…”

Section: Discussionmentioning

confidence: 99%

Expression of Livin and PlGF in human osteosarcoma is associated with tumor progression and clinical outcome

Sun

Chen

et al. 2018

Oncol Lett

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Baculoviral IAP repeat containing 7 (BIRC7/Livin/ML-IAP/KIAP; referred to as Livin throughout the present study) and placental growth factor (PlGF) are not detectable in the majority of normal differentiated tissues, but are present in a number of types of cancer, including hepatocellular carcinoma, ovarian cancer and renal cell carcinoma. The aim of the present study was to assess the expression levels of Livin and PlGF in human osteosarcoma specimens and cell lines, and to analyze the functions of Livin and PIGF in the prognosis of osteosarcoma. The expression levels of Livin and PlGF in 48 osteosarcoma specimens and three osteosarcoma cells were determined using immunohistochemistry and reverse transcription-quantitative polymerase chain reaction. The positivity rates of Livin and PlGF in osteosarcoma specimens were 58.3 and 60.4%, respectively, but were 0% in normal bone tissues. The expression levels of Livin and PlGF were increased in MG-63 cells, compared with those in the other cell lines evaluated in the present study. In addition, the expression levels of Livin and PlGF were significantly associated with tumor diameter and Enneking staging, but were independent of tumor site, age and sex of patients. The expression level of Livin was not associated with PlGF. Furthermore, the 5-year overall survival rate was decreased in the Livin or PlGF expression group, compared with that in the non-expression group (P=0.034 and P=0.012, respectively). The expression levels of Livin and PlGF were independent prognostic factors for patients with osteosarcoma. The results of the present study demonstrated that Livin and PlGF may participate in the pathogenesis of osteosarcoma. Therefore, pharmacological inhibition of Livin or PlGF may provide a novel strategy for osteosarcoma treatment.

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“…Previous studies have linked Livin to metastasis in multiple solid tumors, such as lung cancer, 19 breast cancer, 20 , 21 gastric cancer, 17 and laryngohypopharyngeal cancer. 16 In CRC, ectopic overexpression of Livin correlates with tumor metastasis and implies poor prognosis.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Livin promotes migration and invasion of colorectal cancer cells by induction of epithelial–mesenchymal transition via NF-κB activation

Cao

Wang

et al. 2016

OTT

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Livin is a novel member of the inhibitors of apoptosis protein family and has been implicated in the development and progression of colorectal cancer (CRC). However, the underlying mechanisms of Livin in CRC remain not fully understood. In this study, we investigated the effects of Livin expression on the proliferation and metastasis of CRC cells and also addressed its related molecular mechanism to metastasis. The expression of Livin in CRC cells (HCT116, SW480, and HT-29 cell lines) was determined by Western blot analysis. Our results show that the overexpression of Livin significantly promotes the proliferation, migration, and invasion of SW480 cells. Concurrently, the inhibition of Livin reduces the proliferation, migration, and invasion of HCT116 cells. In addition, Livin overexpression promotes the epithelial–mesenchymal transition, as evidenced by a decrease in epithelial E-cadherin expression and an increase in mesenchymal markers, including vimentin, Slug, and Snail. Furthermore, adding the NF-κB inhibitor, BAY 11-7028, or transfecting with small interfering RNA against p65 notably restores the expression level of E-cadherin and attenuates the invasive ability of Livin-overexpressing cells. Taken together, these results indicate that Livin potentiates migration and invasion of CRC cells partially through the induction of epithelial–mesenchymal transition via NF-κB activation. Livin may be a potential therapeutic target for CRC.

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Silencing of Livin inhibits tumorigenesis and metastasis via VEGF and MMPs pathway in lung cancer

Cited by 22 publications

References 39 publications

miR-205 targets angiogenesis and EMT concurrently in anaplastic thyroid carcinoma

miR-205 targets angiogenesis and EMT concurrently in anaplastic thyroid carcinoma

Expression of Livin and PlGF in human osteosarcoma is associated with tumor progression and clinical outcome

Overexpression of Livin promotes migration and invasion of colorectal cancer cells by induction of epithelial–mesenchymal transition via NF-κB activation

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Silencing of Livin inhibits tumorigenesis and metastasis via VEGF and MMPs pathway in lung cancer

Cited by 22 publications

References 39 publications

miR-205 targets angiogenesis and EMT concurrently in anaplastic thyroid carcinoma

miR-205 targets angiogenesis and EMT concurrently in anaplastic thyroid carcinoma

Expression of Livin and PlGF in human osteosarcoma is associated with tumor progression and clinical outcome

Overexpression of Livin promotes migration and invasion of colorectal cancer cells by induction of epithelial&ndash;mesenchymal transition via NF-&kappa;B activation

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Overexpression of Livin promotes migration and invasion of colorectal cancer cells by induction of epithelial–mesenchymal transition via NF-κB activation