microRNA‐577 suppresses tumor growth and enhances chemosensitivity in colorectal cancer

Jiang, Haiping; Ju, Hui; Zhang, Lin; Lü, Haijun; Kan, Jie

doi:10.1002/jbt.21888

Cited by 57 publications

(34 citation statements)

References 21 publications

(28 reference statements)

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“…Moreover, one study suggested that miR‐577 is downregulated in colorectal cancer specimens and cells. Restoration of miR‐577 significantly suppresses proliferation and induces a G0/G1 cell cycle arrest in colorectal cancer cells . The relative expression of miR‐577 is lower in hepatocellular carcinoma tissues than in ANT.…”

Section: Discussionmentioning

confidence: 98%

MiR‐577 suppresses epithelial‐mesenchymal transition and metastasis of breast cancer by targeting Rab25

et al. 2018

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BackgroundMicroRNAs can act as both tumor suppressor genes and oncogenes and participate in cell proliferation, metastasis, and apoptosis. Low levels of miR‐577 are found in several cancers, for example, thyroid carcinoma, glioblastoma, and hepatocellular carcinoma. The aim of this study was to investigate the effect of miR‐577 on breast cancer (BC).MethodsThe relative level of miR‐577 in 120 BC tissues and cells was detected by real‐time PCR. MDA‐MB‐231 cells with upregulated miR‐577 and MCF‐7 cells with downregulated miR‐577 were established. Transwell invasion assays were used to examine the invasiveness of cells. Epithelial‐mesenchymal transition (EMT) markers were evaluated by immunofluorescence and Western blot. Targeted combinations of miR‐577 and Rab25 were analyzed by luciferase assays. Xenograft models were used to examine the effect of miR‐577 on BC metastasis.Results MiR‐577 expression was significantly suppressed in BC tissues. Tumor size, tumor stage, and lymphatic metastasis were attributed to miR‐577 expression. Moreover, miR‐577 overexpression strongly inhibited the invasiveness and EMT of BC cells in vitro. MiR‐577 directly regulated Rab25 in BC. Rab25 upregulation by miR‐577 decreased the levels of E‐cadherin and increased the levels of Vimentin. Notably, Rab25 knockdown inhibited BC invasion; however, an increase in Rab25 counteracted the invasive effect of miR‐577 in BC.ConclusionResults indicated that miR‐577 suppressed EMT by inhibiting Rab25 expression in BC. MiR‐577 and Rab25 are considered potential targets of BC treatment.

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Section: Discussionmentioning

confidence: 98%

MiR‐577 suppresses epithelial‐mesenchymal transition and metastasis of breast cancer by targeting Rab25

et al. 2018

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“…Increasing evidence indicated that abnormal miRNA expression contributes to the carcinogenesis and progression of multiple human cancers (26)(27)(28). Numerous studies have shed light on tumour-targeting therapies using miRNAs as novel diagnostic and therapeutic tools (29)(30)(31).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-661 promotes non-small cell lung cancer progression by directly targeting RUNX3

Wang

et al. 2017

Molecular Medicine Reports

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Lung cancer is the primary cause of cancer‑associated mortality in men and women worldwide. Increasing evidence indicates that abnormal microRNA (miRNA) expression contributes to the carcinogenesis and progression of multiple human cancers, including non‑small cell lung cancer (NSCLC). Therefore, miRNAs exhibit the potential to act as biomarkers for the diagnosis, treatment and prognosis of human malignancies. miRNA‑661 (miR‑661) has previously been demonstrated to be important in the development of various human cancer types. However, the expression levels, functions and underlying mechanisms of miR‑661 in NSCLC remain to be elucidated. The present study demonstrated that miR‑661 was upregulated in NSCLC tissues and cell lines. In addition, miR‑661 expression levels were significantly correlated with differentiation and tumor stage lymph node metastasis of NSCLC patients. Functional experiments demonstrated that miR-661 downregulation inhibited NSCLC cell proliferation and invasion in vitro. Furthermore, runt‑related transcription factor 3 (RUNX3) was identified as a direct target of miR‑661 in NSCLC. RUNX3 was expressed at a low level in NSCLC tissues and was negatively correlated with the miR‑661 expression level. Further experiments revealed that RUNX3 knockdown significantly rescued the effects of miR‑661 underexpression on NSCLC cell proliferation and invasion. In conclusion, the present findings indicated a role for miR‑661 as an oncogene in NSCLC via direct targeting of RUNX3, thus suggesting that miR‑661 may be used to develop novel therapies for NSCLC patients.

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“…Increasing evidence has revealed the role of HSP27 in 5-FU resistance in colon cancer cells (15)(16)(17)(18)(19)(20). Increased expression of HSP27 resulted in greater resistance to 5-FU in colon cancer cells (18,39), whereas suppression of HSP27 via gene knockdown (16,38) or pharmaceuticals (39,40), enhanced sensitivity to 5-FU. Moreover, HSP27 is associated with VCR resistance in cancer cells (41).…”

Section: Discussionmentioning

confidence: 99%

Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

Liu

Long

et al. 2020

Oncol Lett

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Multidrug resistance in cancer cells is a primary factor affecting therapeutic efficacy. Heat shock 27 kD protein 1 (HSP27) is associated with cell apoptosis and resistance to chemotherapy. However, the mechanisms underlying HSP27-associated pathways in colon cancer cells remain unclear. Therefore, the present study used short hairpin (sh) RNA to inhibit HSP27 expression in colon cancer cells in order to investigate the effects in vitro and in vivo. Flow cytometry was used to investigate cell apoptosis and a xenograft model was employed to examine the tumorigenesis. Protein expression was measured by Western blotting. The results revealed that suppression of HSP27 expression significantly increased cell apoptosis, inhibited tumor growth and enhanced sensitivity to the anti-cancer agents 5-fluorouracil (5-FU) and vincristine (VCR). shHSP27 significantly decreased the expression of notch receptor 1 and the phosphorylation level of Akt and mTOR, and enhanced the effect of 5-FU and VCR. In conclusion, HSP27 suppression enhanced the sensitivity of colon cancer cells to 5-FU and VCR, and increased colon cancer cell apoptosis with and without chemotherapy. Therefore, the development of novel therapeutic agents that inhibit the expression of HSP27 may offer a new treatment option for colon cancer.

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microRNA‐577 suppresses tumor growth and enhances chemosensitivity in colorectal cancer

Cited by 57 publications

References 21 publications

MiR‐577 suppresses epithelial‐mesenchymal transition and metastasis of breast cancer by targeting Rab25

MiR‐577 suppresses epithelial‐mesenchymal transition and metastasis of breast cancer by targeting Rab25

MicroRNA-661 promotes non-small cell lung cancer progression by directly targeting RUNX3

Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

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