MiR‐130b promotes the progression of oesophageal squamous cell carcinoma by targeting <i><scp>SASH</scp>1</i>

Zhu, Yuxing; Ma, Yupo; Peng, Honghua; Gong, Lian; Mengqin, Xiao; Xiang, Lei; He, Deyan; Cao, Ke

doi:10.1111/jcmm.13887

Cited by 17 publications

(14 citation statements)

References 23 publications

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“…Due to late diagnosis, recurrence and metastasis, the overall survival time of patients with ESCC is not satisfactory (1,4). Therefore it is important to identify the molecular mechanisms and develop novel strategies for ESCC therapy (5,6). Recently, some oncogenes have been reported to be responsible for the growth and metastasis of ESCC, and some of them have been suggested to be potential therapeutic targets (7,8).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of cervical carcinoma expressed PCNA regulatory long non‑coding RNA promotes esophageal squamous cell carcinoma progression

et al. 2020

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Cervical carcinoma expressed PCNA regulatory long non-coding (lnc)RNA (CCEPR) has recently been reported to play oncogenic roles in some common types of human cancer. However, the clinical significance of CCEPR mRNA expression levels in esophageal squamous cell carcinoma (ESCC) and the exact function of CCEPR in regulating the malignant phenotypes of ESCC cells have not been previously investigated. In the present study, CCEPR mRNA expression level was upregulated in ESCC tissues and cell lines, and overexpression of CCEPR was associated with advanced TNM stage, lymph node metastasis, and poor prognosis in ESCC. In vitro experiments showed that silencing CCEPR mRNA expression levels significantly suppressed the proliferation, migration, and invasion of ESCC cells, while inducing ESCC cell apoptosis. Furthermore, inhibition of CCEPR decreased the protein expression levels of matrix metalloproteinase (MMP)2 and MMP9 and inhibited epithelial-mesenchymal transition in ESCC cells. In conclusion, the results showed that CCEPR plays an oncogenic role in ESCC and suggests that CCEPR could be used as a potential therapeutic target for ESCC treatment.

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Section: Introductionmentioning

confidence: 99%

Upregulation of cervical carcinoma expressed PCNA regulatory long non‑coding RNA promotes esophageal squamous cell carcinoma progression

et al. 2020

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“…7 SASH1 deficiency was also associated with the increased proliferation and aggressiveness of oesophageal squamous cell carcinoma (ESCC) cells. 19 In addition, the inhibition of SASH1 by miR-17 is involved in the increased cell proliferation, migration and the decreased cell apoptosis in osteosarcoma cells. 20 Thus, SASM1 is closely correlated with the development and progression of tumors and could be regarded as a promising marker for diagnosis and prognosis of malignant neoplasm.…”

Section: Discussionmentioning

confidence: 99%

<p>SASH1 Suppresses the Proliferation and Invasion of Human Skin Squamous Cell Carcinoma Cells via Inhibiting Akt Cascade</p>

Chen¹,

Yang²,

Lei³

et al. 2020

OTT

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The SAM-and SH3-domain containing 1 gene (SASH1) has been considered as a tumor suppressor in some cancers. Nevertheless, the effect of SASH1 on the proliferation and invasion of human skin squamous cell carcinoma (cSCC) remains poorly understood. Therefore, the purpose of the present study was to observe the potential role of SASH1 in cSCC and investigate its underlying mechanisms. Methods: The overexpression of SASH1 was constructed by transfecting the pcDNA3.1/ SASH1 vector into SCL-1 and A431 cells, and SASH1 knockdown was generated by transfecting the SASH1 siRNA into cSCC cells. Then, cell proliferation, invasion, apoptosis, and Akt pathway were observed. Results: The expression levels of SASH1 mRNA and protein were greatly reduced in cSCC cells. The overexpression of SASH1 inhibited the viability and invasion of cSCC cells, while its knockdown induced the viability and invasion of cSCC cells. The overexpression of SASH1 also suppressed the expression levels of p-Akt and its target genes, including cyclin D1, Bcl-2, and metal matrix proteinase 2(MMP-2). By contrast, SASH1 knockdown exerted the opposite role. Furthermore, inhibition of Akt obviously decreased the inducible effect of cSCC knockdown on the proliferation and invasion of cSCC cells. Conclusion:Overall, these results found that SASH1 inhibits the proliferation and invasion of cSCC cells via suppressing Akt cascade, indicating a tumor inhibitory effect of SASH1 in cSCC cells.

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“…In our recently published paper, we investigated miR-124-5p, which existed in MSCs-conditioned medium, and found that the miR-124-5p was involved in the regulation of MSCs-conditioned medium in LPS-induced ALI by targeting α-ENaC [19]. Related studies have shown that miR-130b in MSCs can regulate the inflammatory response, cell function and gene expression of various diseases [20][21][22], whereas its role in ALI and the relative mechanisms are seldom studied. Therefore, we chose miR-130b as our main research object and co-cultured with AT2 cells to explore its role in the regulation of MSCs in LPS-induced ALI, aiming to provide a novel direction for therapeutic strategy in ALI.…”

Section: Introductionmentioning

confidence: 99%

Bone Marrow Mesenchymal Stem Cells Derived miRNA-130b Enhances Epithelial Sodium Channel by Targeting PTEN

Zhang¹,

Hong²,

Liu³

et al. 2020

Preprint

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Aims: Acute lung injury (ALI) is a clinical syndrome with high morbidity and mortality, and severe pulmonary edema is one of the characteristics of ALI. Epithelial sodium channel (ENaC) located on the apical side of alveolar type 2 epithelial (AT2) cells is the primary rate limiting segments in alveolar fluid clearance. Many preclinical studies have revealed that mesenchymal stem cells (MSCs) based therapy has great therapeutic potential for ALI, while the role of ENaC in this process is rarely known. Methods: We studied the effects of bone marrow-derived MSCs (BMSCs) on the protein/mRNA expression and activity of ENaC in primary mouse AT2 and H441 cells by co-culture with them, respectively. Moreover, the changes of miRNA-130b in AT2 cells were detected by qRT-PCR, and we studied the involvement of phosphatase and tensin homolog deleted on chromosome ten (PTEN) in miRNA-130b regulated ENaC. Results: Our results demonstrated that BMSCs could increase the expression of miRNA-130b, which showed adverse effects on the protein expression of α/γ-ENaC and PTEN in AT2 cells. SiRNA-mediated downregulation of PTEN could increase the protein expression of α/γ-ENaC in AT2 cells, supporting PTEN as a negative regulator of ENaC. Conclusion: In summary, miRNA-130b in BMSCs can enhance ENaC at least partially by targeting PTEN, which may provide a promising new direction for therapeutic strategy in ALI.

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MiR‐130b promotes the progression of oesophageal squamous cell carcinoma by targeting SASH1

Cited by 17 publications

References 23 publications

Upregulation of cervical carcinoma expressed PCNA regulatory long non‑coding RNA promotes esophageal squamous cell carcinoma progression

Upregulation of cervical carcinoma expressed PCNA regulatory long non‑coding RNA promotes esophageal squamous cell carcinoma progression

<p>SASH1 Suppresses the Proliferation and Invasion of Human Skin Squamous Cell Carcinoma Cells via Inhibiting Akt Cascade</p>

Bone Marrow Mesenchymal Stem Cells Derived miRNA-130b Enhances Epithelial Sodium Channel by Targeting PTEN

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