MicroRNA-335 and its target Rock1 synergistically influence tumor progression and prognosis in osteosarcoma

Wang, Yong; Wang, Ningning; Zeng, Xiandong; Sun, Jie; Wang, Guangbin; Xu, Hui; Zhao, Wei

doi:10.3892/ol.2017.5818

Cited by 28 publications

(20 citation statements)

References 32 publications

(30 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Despite the identification of a number of miRNA targets involved in human tumors, in the majority of cases their mechanisms of effect remain unclear. The expression of miR‐335 has been shown to be aberrant in tumor tissue from several types of cancer, and is associated with cell proliferation and inflammation . The present study found that miR‐335 was downregulated in NSCLC tumor tissues compared with adjacent non‐tumor tissues.…”

Section: Discussionsupporting

confidence: 52%

miR‐335 inhibited cell proliferation of lung cancer cells by target Tra2β

et al. 2017

View full text Add to dashboard Cite

Accumulating evidence has suggested that the dysregulation of miRNA is an important factor in the pathogenesis of lung cancer. Here, we demonstrate that miR‐335 expression is reduced in non‐small cell lung cancer (NSCLC) tumors relative to non‐cancerous adjacent tissues, while the expression of Tra2β is increased. In addition, clinical data revealed that the increased Tra2β and decreased miR‐335 expression observed in NSCLC cells was associated with poor patient survival rates. In vitro experimentation showed that the overexpression of miR‐335 inhibited the growth, invasion and migration capabilities of A459 lung cancer cells, by targeting Tra2β. In contrast, inhibition of miR‐335 or overexpression of the Tra2β target gene stimulated the growth, invasion and migratory capabilities of A459 lung cancer cells in vitro. Furthermore, overexpression of miR‐335 or inhibition of Tra2β decreased the phosphorylation of Rb‐S780 and Rb‐AKT. Overall, these findings suggest that the downregulation of miR‐335 in A459 lung cancer cells promoted cell proliferation through upregulation of Tra2β, mediated via activation of the AKT/mTOR signaling pathway, and suggest that miR‐335 may have potential as a novel therapeutic target for NSCLC.

show abstract

Section: Discussionsupporting

confidence: 52%

miR‐335 inhibited cell proliferation of lung cancer cells by target Tra2β

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Among all of the downregulated miRNAs, miR-129 and -335 showed the most significant changes. miR-129 and -335 play key roles in tumorigenesis (20)(21)(22)(23), whereas their roles in wound healing remain unknown. In this study, in diabetic conditions induced by AGE-BSA treatment, miR-129 and -335 expression significantly decreased in HaCaT cells and primary cultured keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

“…We used serum miRNA expression profiling to identify novel miRNAs in diabetic wounds and found that microRNA-129 (miR-129) and miR-335 were significantly downregulated in patients with diabetes compared with healthy patients. miR-129 and -335 play key roles in the regulation of cancer progression, chemoresistance, proliferation, and cell cycle control (20)(21)(22)(23). However, their function in diabetic wound healing is unclear.…”

mentioning

confidence: 99%

MicroRNA-129 and -335 Promote Diabetic Wound Healing by Inhibiting Sp1-Mediated MMP-9 Expression

et al. 2018

View full text Add to dashboard Cite

Diabetic wounds are recalcitrant to healing. However, the mechanism causing this dysfunction is not fully understood. High expression of matrix metalloproteinase-9 (MMP-9) is indicative of poor wound healing. In this study, we show that specificity protein-1 (Sp1), a regulator of MMP-9, binds directly to its promoter and enhances its expression. Additionally, we demonstrated that Sp1 is the direct target of two microRNAs (miRNAs), miR-129 and -335, which are significantly downregulated in diabetic skin tissues. In vitro experiments confirmed that miR-129 or -335 overexpression inhibits MMP-9 promoter activity and protein expression by targeting Sp1, whereas the inhibition of these miRNAs has the opposite effect. The beneficial role of miR-129 or miR-335 in diabetic wound healing was confirmed by the topical administration of miRNA agomirs in diabetic animals. This treatment downregulated Sp1-mediated MMP-9 expression, increased keratinocyte migration, and recovered skin thickness and collagen content. The combined treatment with miR-129 and miR-335 induced a synergistic effect on Sp1 repression and MMP-9 downregulation both in vitro and in vivo. This study demonstrates the regulatory mechanism of Sp1-mediated MMP-9 expression in diabetic wound healing and highlights the potential therapeutic benefits of miR-129 and -335 in delayed wound healing in diabetes.

show abstract

“…All the procedures were carried out as described . In brief, tissue slides (4 µm thick) were firstly incubated with the MK2, TNF‐α, and IL‐6 primary antibodies at 4°C overnight respectively, then subsequently incubated with biotinylated secondary antibodies (2 μg/mL, Abcam) at 37°C for 30 min.…”

Section: Methodsmentioning

confidence: 99%

MiR‐137 inhibited inflammatory response and apoptosis after spinal cord injury via targeting of MK2

Gao

Dai²,

Feng

et al. 2017

J of Cellular Biochemistry

View full text Add to dashboard Cite

Spinal cord injuries are common and troublesome disorder, which is mediated by various signal pathways and mechanisms. MK2 is also involved in numerous inflammatory diseases including spinal cord injury. The role of microRNA-137 (miR-137) and its detailed working mechanism in spinal cord injuries remain unclear. In the present study, we found that an elevated MK2 but a decreased miR-137 was expressed in serum specimens of patients with spinal cord injury and in hydrogen peroxide-treated C8-D1A and C8-B4 cells. Meanwhile, we suggested that upregulation of miR-137 could inhibit the expression of TNF-α and IL-6, two markers of inflammatory response after SCI, and apoptosis in hydrogen peroxide-treated C8-D1A and C8-B4 cells. Furthermore, we verified that MK2 was a direct target of miR-137 thorough a constructed luciferase assay. Even further, we elucidated that miR-137 could suppress the inflammatory response and apoptosis via negative regulation of MK2. Finally, through an animal model trial performed using mice, we demonstrated the protective effect of how miR-137 works on inflammatory response and apoptosis after spinal cord injury. Considering all the forementioned, our findings revealed that miR-137 inhibited inflammatory response and apoptosis after spinal cord injury via the targeting of MK2. The outcomes of the present study might indicate a new target in molecular treatment of SCI.

show abstract

MicroRNA-335 and its target Rock1 synergistically influence tumor progression and prognosis in osteosarcoma

Cited by 28 publications

References 32 publications

miR‐335 inhibited cell proliferation of lung cancer cells by target Tra2β

miR‐335 inhibited cell proliferation of lung cancer cells by target Tra2β

MicroRNA-129 and -335 Promote Diabetic Wound Healing by Inhibiting Sp1-Mediated MMP-9 Expression

MiR‐137 inhibited inflammatory response and apoptosis after spinal cord injury via targeting of MK2

Contact Info

Product

Resources

About