miR-143-3p targeting of ITGA6 suppresses tumour growth and angiogenesis by downregulating PLGF expression via the PI3K/AKT pathway in gallbladder carcinoma

Jin, Yunpeng; Hu, Yunping; Wu, Xiangsong; Wu, Yaoshi; Ye, Yuanyuan; Li, Huai-Feng; Liu, Yongchen; Jiang, Lin; Liu, Fa-Tao; Zhang, Yi-Jian; Hao, Yajuan; Liu, Xiyong; Liu, Yingbin

doi:10.1038/s41419-017-0258-2

Cited by 88 publications

(66 citation statements)

References 35 publications

(42 reference statements)

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“…LKB1 inhibits GBC cell progression via the JAK/STAT3 cascade. Several signaling pathways, including JAK/STAT3, PI3K/Akt, MEK/ERK and EMT have been reported to play a role in the proliferation of GBC cells (27)(28)(29)(30)(31)(32). In this study, our data demonstrated that PI3K/Akt and MEK/ERK pathways, and EMT were not affected by LKB1 overexpression, while the phosphorylation of the STAT3 molecule was evidently activated in both the SGC-996 and GBC-SD LKB1 control cells (Fig.…”

Section: Downregulation Of Lkb1 In Gbc Cscssupporting

confidence: 52%

Tumor suppressor LKB1 inhibits the progression of gallbladder carcinoma and predicts the prognosis of patients with this malignancy

Wang

et al. 2018

Int J Oncol

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Gallbladder carcinoma (GBC) represents the most common fatal tumors of the biliary tract. The 3-year or 5-year survival rate for patients with this disease are 30 and 5%, respectively. Liver kinase B1 (LKB1), a primary upstream kinase of adenosine monophosphate-activated protein kinase (AMPK) necessary for maintaining cell metabolism and energy homeostasis, has been found to be an important tumor suppressor gene in recent years, and its inactivation has also found to be closely associated with tumor growth, metastasis and cancer stem cell (CSC) proliferation. Nevertheless, the function of LKB1 in GBC remains unclear. In this study, we found that the expression of LKB1 in GBC tissues was decreased compared with that in non-cancerous tissues. LKB1 overexpression suppressed the proliferation, metastasis and expansion of GBC CSCs. Mechanically, LKB1 suppressed GBC cell progression via the JAK/signal transducer and activator of transcription 3 (STAT3) pathway. The use of the JAK2 inhibitor, AZD‑1480, attenuated the suppressive effects of LKB1 overexpression on the growth, metastasis and self-renewal ability of the GBC cells, which further demonstrated that JAK/STAT3 was involved in the LKB1-induced suppression of GBC cell growth, metastasis and self-renewal ability. More importantly, the decreased expression of LKB1 was a predictor of a poor prognosis of patients with GBC. On the whole, our data indicate that LKB1 inhibits GBC cell growth, metastasis and self-renewal ability by disrupting JAK/STAT3 signaling, and may thus prove to be a novel prognostic biomarker for patients with GBC.

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Section: Downregulation Of Lkb1 In Gbc Cscssupporting

confidence: 52%

Tumor suppressor LKB1 inhibits the progression of gallbladder carcinoma and predicts the prognosis of patients with this malignancy

Wang

et al. 2018

Int J Oncol

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“…Our results appear to support the idea that miR-143-3p acts as a tumor suppressor due to its effects on cell metastasis and invasion via targeting ITGA6. Jin et al 34 also indicated that miR-143-3p could suppress tumor growth and angiogenesis by targeting ITGA6 and PLGF through the PI3K/AKT pathway in gallbladder carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of lncRNA ADAMTS9-AS2 Promotes Salivary Adenoid Cystic Carcinoma Metastasis via PI3K/Akt and MEK/Erk Signaling

Xie

et al. 2018

Molecular Therapy

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Neurotropic infiltrative growth and distant metastasis are the main causes of death in salivary adenoid cystic carcinoma (SACC) patients. Long noncoding RNAs (lncRNAs) are involved in many human neoplasms, however, their potential roles in SACC are unclear. In our study, we found that ADAM metallopeptidase with thrombospondin type 1 motif, 9 (ADAMTS9) antisense RNA 2 (ADAMTS9-AS2) was significantly upregulated in SACC patients with metastasis and SACC-lung metastasis (LM) cells. Moreover, ADAMTS9-AS2 expression was closely associated with the prognosis and distant metastasis in SACC patients. Next, we found that c-myc could specifically bind to the promoter of ADAMTS9-AS2 and activated its transcription. Knockdown of ADAMTS9-AS2 significantly inhibited migration and invasion of SACC cells in vitro and distant lung metastasis in vivo. Furthermore, ADAMTS9-AS2, which mainly expressed in the cytoplasm, shared microRNA (miRNA) response elements with Integrin α6 (ITGA6). Overexpression of ADAMTS9-AS2 competitively bound to miR-143-3p that inhibited ITGA6 from miRNA-mediated degradation, and thus it activated the activity of PI3K/Akt and MEK/Erk signaling and facilitated SACC metastasis. In summary, ADAMTS9-AS2 promotes migration and invasion in SACC by competing with miR-143-3p. This sheds a new insight into the regulation mechanism of ADAMTS9-AS2, and it provides a possible application for the SACC treatment.

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“…According to Zhang and colleagues, miR-33a was down-regulated in human GBC tissues, which functioned as a tumor suppressor in GBC by targeting Twist [14]. Jin et al found that miR-143-3p was down-regulated in GBC tumor tissues and was an inhibitor of GBC progression [17]. Hence, miRNAs may be used as therapeutic markers for GBC [18].…”

Section: Discussionmentioning

confidence: 99%

MiR-520b inhibits proliferation, migration and invasion in gallbladder carcinoma by targeting RAB22A

et al. 2021

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Introduction: Previous studies have reported that miR-520b exhibited inhibitory effects on various human tumors, whereas the effects of miR-520b on gallbladder carcinoma (GBC) have remained unclear. To investigate the effects of miR-520b on GBC progression and reveal the underlying mechanisms, this study was performed. Material and methods: MiR-520b and RAB22A mRNA levels were analyzed by quantitative real-time PCR (qPCR). RAB22A protein level was analyzed via Western blot and immunohistochemical (IHC) analysis. The proliferation, colony formation ability, migration and invasion of NOZ cells were measured via MTT, colony formation, wound healing and transwell invasion assay respectively. Results: MiR-520b expression level was lower in human GBC tissues than that in neighboring normal tissues. MiR-520b mimic repressed NOZ cell proliferation, colony formation ability, migration and invasion, whereas miR-520b inhibitor exhibited opposite effects. Dual luciferase reporter assay confirmed that miR-520b could bind to the 3′-untranslated regions of RAB22A mRNA. Moreover, RAB22A overexpression significantly abolished the anti-tumor effects of miR-520b in a NOZ cell model. Western blot, qPCR and IHC analysis proved that human GBC tissues showed a higher RAB22A expression level than neighboring normal tissues. Additionally, there was a negative association between miR-520b and RAB22A expression. Conclusions: MiR-520b had suppressive effects on GBC via targeting RAB22A in vitro.

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miR-143-3p targeting of ITGA6 suppresses tumour growth and angiogenesis by downregulating PLGF expression via the PI3K/AKT pathway in gallbladder carcinoma

Cited by 88 publications

References 35 publications

Tumor suppressor LKB1 inhibits the progression of gallbladder carcinoma and predicts the prognosis of patients with this malignancy

Tumor suppressor LKB1 inhibits the progression of gallbladder carcinoma and predicts the prognosis of patients with this malignancy

Upregulation of lncRNA ADAMTS9-AS2 Promotes Salivary Adenoid Cystic Carcinoma Metastasis via PI3K/Akt and MEK/Erk Signaling

MiR-520b inhibits proliferation, migration and invasion in gallbladder carcinoma by targeting RAB22A

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