The Tumor Suppressor Roles of miR-433 and miR-127 in Gastric Cancer

Guo, Li; Li, Hui; Wang, Fang; Yu, Jia; He, Jin‐Sheng

doi:10.3390/ijms140714171

Cited by 100 publications

(84 citation statements)

References 29 publications

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“…miR-433 has been demonstrated to be downregulated in several types of cancer tissue, including (10,(12)(13)(14)16). Consistent with this, the results of the present study also demonstrated the downregulation of miR-433 in breast cancer tissues, which suggests that miR-433 may be tumor-suppressive in breast cancer tissues.…”

Section: Discussionsupporting

confidence: 80%

“…However, caution must be exercised as miR-433 may have downstream targets other than AKT3. Previous studies have found that miR-433 targets Notch1, CREB1, PAX6, HDAC6, KRAS and c-Met in other types of cancer (10,12,13,16). Therefore, future studies must assess other targets of miR-433 in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies have demonstrated that miRNAs can perform oncogenic or tumor suppressive roles in various types of cancers. Previous studies have demonstrated the functional roles of miR-433 in several types of cancer, including retinoblastoma (10), ovarian cancer (11), bladder cancer (11), oral squamous cell carcinoma (OSCC) (12), gastric cancer (13), hepatocellular carcinoma (HCC) (14) and lung cancer (15). The downstream targets of miR-433 have been revealed to be strongly associated with cancer development, including Notch1, cAMP responsive element binding protein 1 (CREB1), paired box protein Pax-6 (PAX6), histone deacetylase 6 (HDAC6), kirsten rat sarcoma viral oncogene homolog and hepatocyte growth factor receptor (c-Met) (10,12,13,16 4 and CHANGSHENG YE to be downregulated in these cancer types, and miR-433 was demonstrated to function as a tumor suppressor by inhibiting cell proliferation, migration and differentiation (10,(12)(13)(14)16).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-433 targets AKT3 and inhibits cell proliferation and viability in breast cancer

Wang

et al. 2018

Oncol Lett

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Abstract. Breast cancer is the most frequently diagnosed malignancy in women. However, the molecular mechanisms underlying breast cancer pathogenesis are not fully understood. The present study examined the role of miR-433 in breast cancer and investigated its underlying molecular mechanisms of action. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were performed to analyze the level of microRNA (miRNA/miR)/mRNA and protein expression, respectively. Additionally, MTT assay was used to determined cell proliferation and viability. Cell apoptosis was measured by flow cytometry. A dual-luciferase reporter assay was used to confirm the identity of the downstream target of miR-433. The results revealed that miR-433 was downregulated in breast cancer tissues and cell lines. Overexpression of miR-433 inhibited cell proliferation and cell viability in BT-549 cells, whereas downregulation of miR-433 increased cell proliferation and cell viability in MDA-MB-231 cells. Further flow cytometry analysis revealed that miR-433 was able to induce apoptosis and also alter the levels of proteins expression of B-cell lymphoma-2 and Bcl-associated X. Bioinformatics analysis showed that RAC-γ serine/threonine-protein kinase (AKT3) was one of the downstream targets of miR-433, and luciferase reporter assay further confirmed that AKT3 is a direct target of miR-433. The knockdown of AKT3 was able to inhibit proliferation and viability in BT-549 cells. Overexpression of AKT3 prevented the inhibitory effects of miR-433 on proliferation and viability in BT-549 cells. The level of AKT3 mRNA expression was upregulated in breast cancer tissues compared with normal tissues and was inversely correlated with miR-433 expression levels. In summary, the results of the present study results indicate that the tumor-suppressive role of miR-433 may be mediated by regulating AKT3. miR-433 may therefore serve as a potential therapeutic target for breast cancer.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA-433 targets AKT3 and inhibits cell proliferation and viability in breast cancer

Wang

et al. 2018

Oncol Lett

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“…The present data, along with an analysis of a published dataset (27), showed that miR-433 was overexpressed in osteosarcoma tissues and cell lines. In combi nation with previous reports revealing the roles of miR-433 in various other types of cancer, including ovarian and gastric cancer (28,29), the present study further confirmed that miR-433 functions as an oncomiR in osteosarcoma. Furthermore, overexpression of miR-433 was shown to decrease the apoptosis of osteosarcoma cells by targeting PDCD4 in vitro.…”

Section: Discussionsupporting

confidence: 74%

“…For example, the overexpression of miR-433 in a gastric cancer cell line suppressed cell growth and invasion by downregulating KRAS expression (8). Overexpression of miR-433 downregulated thymidylate synthetase mRNA and protein expression and enhanced the sensitivity of HeLa cells to 5-fluorouracil (9).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-433 regulates apoptosis by targeting PDCD4 in human osteosarcoma cells

Sun

Wang

et al. 2017

Oncology Letters

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Abstract. Osteosarcoma is the most common aggressive sarcoma of the bone in children and adolescents. It is characterized by a high level of genetic instability and recurrent DNA deletions and amplifications. microRNAs (miRNAs) play a key role in cancer initiation, progression and metastasis; however, the potential role of miRNAs in osteosarcoma remains largely unknown. In the present study, miR-433 was shown to be overexpressed in osteosarcoma tissues compared with normal human osteoblasts. Transfection of miR-433 mimics into osteosarcoma cell lines significantly decreased apoptosis by targeting programmed cell death 4, a tumor suppressor that is involved in apoptosis. In contrast, inhibition of miR-433 enhanced apoptosis. Furthermore, in vivo miR-433 overexpression inhibited the apoptosis of tumor cells and increased tumor growth. The results of the present study suggested that miR-433 is a potential molecular target for osteosarcoma therapy.

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MAPK4 facilitates angiogenesis by inhibiting the ERK pathway in non‐small cell lung cancer

Chen,

Yang,

Liu

et al. 2024

Cancer Innovation

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BackgroundAngiogenesis plays an important role in the occurrence and development of non‐small cell lung cancer (NSCLC). The atypical mitogen‐activated protein kinase 4 (MAPK4) has been shown to be involved in the pathogenesis of various diseases. However, the potential role of MAPK4 in the tumor angiogenesis of NSCLC remains unclear.MethodsAdult male C57BL/6 wild‐type mice were randomly divided into the control group and p‐siMAPK4 intervention group, respectively. The cell proliferation was analyzed with flow cytometry and immunofluorescence staining. The vascular density in tumor mass was analyzed by immunofluorescence staining. The expressions of MAPK4 and related signaling molecules were detected by western blot analysis and immunofluorescence staining, and so on.ResultsWe found that the expression of MAPK4, which was dominantly expressed in local endothelial cells (ECs), was correlated with tumor angiogenesis of NSCLC. Furthermore, MAPK4 silencing inhibited the proliferation and migration abilities of human umbilical vein ECs (HUVECs). Global gene analysis showed that MAPK4 silencing altered the expression of multiple genes related to cell cycle and angiogenesis pathways, and that MAPK4 silencing increased transduction of the extracellular regulated protein kinases 1/2 (ERK1/2) pathway but not Akt and c‐Jun n‐terminal kinase pathways. Further analysis showed that MAPK4 silencing inhibited the proliferation and migration abilities of HUVECs cultured in tumor cell supernatant, which was accompanied with increased transduction of the ERK1/2 pathway. Clinical data analysis suggested that the higher expression of MAPK4 and CD34 were associated with poor prognosis of patients with NSCLC. Targeted silencing of MAPK4 in ECs using small interfering RNA driven by the CD34 promoter effectively inhibited tumor angiogenesis and growth of NSCLC in vivo.ConclusionOur results reveal that MAPK4 plays an important role in the angiogenesis and development of NSCLC. MAPK4 may thus represent a new target for NSCLC.

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The Tumor Suppressor Roles of miR-433 and miR-127 in Gastric Cancer

Cited by 100 publications

References 29 publications

MicroRNA-433 targets AKT3 and inhibits cell proliferation and viability in breast cancer

MicroRNA-433 targets AKT3 and inhibits cell proliferation and viability in breast cancer

MicroRNA-433 regulates apoptosis by targeting PDCD4 in human osteosarcoma cells

MAPK4 facilitates angiogenesis by inhibiting the ERK pathway in non‐small cell lung cancer

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