Homeobox A9 directly targeted by miR‐196b regulates aggressiveness through nuclear Factor‐kappa B activity in non‐small cell lung cancer cells

Yu, Seong‐Lan; Lee, Dong Chul; Sohn, Hyun Ahm; Lee, Soo Young; Jeon, Hyo Sung; Lee, Joon‐Hyung; Park, Chang Gyo; Lee, Hoi Young; Yeom, Young Il; Son, Ji Woong; Yoon, Yoo Sang; Kang, Jaeku

doi:10.1002/mc.22439

Cited by 43 publications

(49 citation statements)

References 51 publications

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“…Studies have shown that HoxA9 accelerated restoration of endothelial damage [16]. Except for the protective effects of HoxA9 on the endothelium, Hox A9 has also been reported to promote E-cadherin expression [17]. Furthermore, HOXA9 potently attenuated the expression of matrix metallopeptidase 9 (MMP 9) by controlling the binding of nuclear factor-kappa B to the promoter of MMP 9 genes, respectively [17].…”

Section: Discussionmentioning

confidence: 99%

“…Except for the protective effects of HoxA9 on the endothelium, Hox A9 has also been reported to promote E-cadherin expression [17]. Furthermore, HOXA9 potently attenuated the expression of matrix metallopeptidase 9 (MMP 9) by controlling the binding of nuclear factor-kappa B to the promoter of MMP 9 genes, respectively [17]. It has been suggested that HoxA9 within the lung may therefore play a critical role in contributing to the regulation of alveolar-capillary permeability and promoting lung repair.…”

Section: Discussionmentioning

confidence: 99%

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Mesenchymal Stem Cells Promoted Lung Wound Repair through Hox A9 during Endotoxemia-Induced Acute Lung Injury

Xin

Liu

Zhu

et al. 2017

Stem Cells International

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Objectives. Acute lung injury (ALI) is a common clinical critical disease. Stem cells transplantation is recognized as an effective way to repair injured lung tissues. The present study was designed to evaluate the effects of mesenchymal stem cells (MSCs) on repair of lung and its mechanism. Methods. MSCs carrying GFP were administrated via trachea into wild-type SD rats 4 hours later after LPS administration. The lung histological pathology and the distribution of MSCs were determined by HE staining and fluorescence microscopy, respectively. Next, differentially expressed HOX genes were screened by using real-time PCR array and abnormal expression and function of Hox A9 were analyzed in the lung and the cells. Results. MSCs promoted survival rate of ALI animals. The expression levels of multiple HOX genes had obvious changes after MSCs administration and HOX A9 gene increased by 5.94-fold after MSCs administration into ALI animals. HOX A9 was distributed in endothelial cells and epithelial cells in animal models and overexpression of Hox A9 can promote proliferation and inhibit inflammatory adhesion of MSCs. Conclusion. HoxA9 overexpression induced by MSCs may be closely linked with lung repair after endotoxin shock.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cells Promoted Lung Wound Repair through Hox A9 during Endotoxemia-Induced Acute Lung Injury

Xin

Liu

Zhu

et al. 2017

Stem Cells International

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“…Lung cancer is one of the most common malignancies and remains the leading cause of cancer-related deaths worldwide [1]. In the various histological subtypes, non-small cell lung cancer (NSCLC) is the most prevalent subtype, which accounts for approximately 80% in all cases of diagnosed with lung cancer [1, 2].…”

Section: Introductionmentioning

confidence: 99%

“…In the various histological subtypes, non-small cell lung cancer (NSCLC) is the most prevalent subtype, which accounts for approximately 80% in all cases of diagnosed with lung cancer [1, 2]. NSCLC is characterized by a high mortality, and the overall five-year survival rate remains less than 15% [2].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, Bhatia et al also found that the role of miR-196b as tumor suppressor in blood cancers [14, 15]. In lung cancer, recent studies showed that miR-196b promoted cell invasion and induced epithelial mesenchymal transition (EMT) process in NSCLC cells [1, 16]. Simultaneously, Tellez et al found that miR-196b as a tumor suppressor whose silencing early in lung carcinogenesis might provide a selective growth advantage to pre-malignant cells [17].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-196b Inhibits Cell Growth and Metastasis of Lung Cancer Cells by Targeting Runx2

Bai

Lin

Sun

et al. 2017

Cell Physiol Biochem

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Background/Aims: Lung cancer is one of the most common causes of cancer related deaths worldwide. The role of several microRNAs (miRNAs) including miR-196b in different cancers has already been established. The study was aimed to explore the role of miR-196b in lung cancer and its possible underlying mechanism. Methods: Human lung cancer cell line A549 was transfected with miR-196b mimic, miR-196b inhibitor and corresponding controls. Then cell viability, migration, invasion, and apoptosis of A549 lung cancer cells either with overexpression or with suppression of miR-196b were estimated sequentially. Next, dual luciferase activity assay was performed to clarify whether Runx2 was a direct target of miR-196b. Finally, the expressions of main factors associated with epithelial mesenchymal transition (EMT), PI3K/AKT/GSK3β, Smad, and JNK pathways were detected by western blot. Results: MiR-196b expression was significantly decreased in A549, H1650 and H1299 cell lines compared with in WI-38 and HEL-1 cell lines. Overexpression of miR-196b suppressed cell viability, migration, invasion, and induced apoptosis as well as inhibited TGF-β induced EMT process in A549 cells. In addition, Runx2 was a putative target of miR-196b, and Runx2 silence remarkably increased cell apoptosis and abolished the promotive effects of miR-196b suppression on cell viability, migration and invasion. Finally, miR-196b also mediated its action by inactivation of PI3K/AKT/GSK3β, Smad, and JNK pathways by down-regulation of Runx2. Conclusion: MiR-196b functions as a tumor suppressor that inhibited cell growth and metastasis of lung cancer cells by targeting Runx2. These findings provided further evidences for treatment of lung cancer.

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HOXA9 is critical in the proliferation, differentiation, and malignancy of leukaemia cells both in vitro and in vivo

Chen

Yu²,

et al. 2017

Cell Biochemistry & Function

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Progress in the understanding of the molecular mechanism for acute myeloid leukaemia is of great significance to generate new potential targets for treatment. Recent studies showed that HOXA9, a homeodomain-containing transcription factor, is commonly deregulated in acute leukaemia. In this study, we elucidated the direct correlation between HoxA9 expression and progression of leukaemia using 2 different types of leukaemia cells HL-60 and MOLT-3. The HoxA9 expression level was decreased in leukaemia cells with the treatment of all-trans retinoic acid or arsenic trioxide (As O ). Downregulation of HoxA9 could impair the proliferation and promote the leukaemia cell death. HoxA9 silencing also potentiated the differentiation of leukaemia cells, and in vivo studies demonstrated that HoxA9 downregulation could interfere the tumour growth. Interestingly, HoxA9 silencing also led to the alteration in miRNA expression, mediating the promoting effect on the leukaemia cell differentiation. Therefore, this work provided a promising and potentially efficient target to leukaemia treatment, indicating that HoxA9 is likely to be an ideal candidate in the gene therapy against acute myeloid leukaemia. In this study, we elucidated the critical role of HoxA9 in the proliferation and differentiation of leukaemia cells both in vitro and in vivo. The effect of HoxA9 modulation was correlated with the clinical effect of all-trans retinoic acid and As O . Furthermore, HoxA9 also regulated the miRNA expression, controlling the leukaemia cell differentiation. Therefore, this work provided new insights into molecular mechanism underlying the leukaemia treatment, potentially putting forward a brand new target to the gene therapy against leukaemia.

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Homeobox A9 directly targeted by miR‐196b regulates aggressiveness through nuclear Factor‐kappa B activity in non‐small cell lung cancer cells

Cited by 43 publications

References 51 publications

Mesenchymal Stem Cells Promoted Lung Wound Repair through Hox A9 during Endotoxemia-Induced Acute Lung Injury

Mesenchymal Stem Cells Promoted Lung Wound Repair through Hox A9 during Endotoxemia-Induced Acute Lung Injury

MicroRNA-196b Inhibits Cell Growth and Metastasis of Lung Cancer Cells by Targeting Runx2

HOXA9 is critical in the proliferation, differentiation, and malignancy of leukaemia cells both in vitro and in vivo

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