miR-326 reverses chemoresistance in human lung adenocarcinoma cells by targeting specificity protein 1

Li, Jipeng; Li, Shanfeng; Chen, Zhe; Wang, Jianhua; Chen, Ying; Xu, Zhengyang; Jin, Man-Wen; Yu, Wanjun

doi:10.1007/s13277-016-5244-2

Cited by 47 publications

(34 citation statements)

References 31 publications

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“…Wu et al (23) reported that miR-326 re-expression attenuated cell growth and motility and promoted cell apoptosis and cell cycle-arrest in colorectal cancer. Studies revealed that miR-326 decreased cell proliferation, viability, colony formation, migration and invasion, reversed chemoresistance and increased apoptosis and epithelial-to-mesenchymal transition of lung cancer (25,(44)(45)(46). These findings indicated that miR-326 could be developed as a therapeutic target for these human cancer types.…”

Section: Discussionmentioning

confidence: 94%

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MicroRNA-326 inhibits melanoma progression by targeting KRAS and suppressing the AKT and ERK signalling pathways

Kang

Zhang

et al. 2017

Oncol Rep

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Abstract. Melanoma is the seventh most common malignancy in females and the fifth most common cancer in males worldwide. An increasing number of studies have reported that microRNA (miRNA) dysregulation is frequently observed in various types of human cancers, including melanoma. Abnormally expressed miRNAs play an important role in melanoma formation and progression by serving as potential biomarkers and therapeutic targets. Recently, miRNA-326 (miR-326) has been reported to be differentially expressed in various types of tissues and play important roles in tumourigenesis and tumour development. However, the expression levels, biological roles and underlying mechanisms of miR-326 in melanoma remain unknown. In the present study, we demonstrated that miR-326 was significantly downregulated in melanoma tissues and cell lines. Functional assays revealed that the enforced expression of miR-326 suppressed melanoma cell proliferation and invasion and increased cell apoptosis in vitro. Using bioinformatic analysis, Kirsten rat sarcoma viral oncogene homolog (KRAS) was predicted as a potential target of miR-326. Luciferase reporter assay confirmed that miR-326 could directly target the 3'-untranslated region of KRAS. In addition, reverse transcription-quantitative polymerase chain reaction and western blot analysis revealed that miR-326 upregulation decreased the KRAS expression in melanoma cells at both the mRNA and protein level. Furthermore, KRAS was upregulated in melanoma tissues and inversely correlated with miR-326 expression. In addition, the KRAS knockdown phenocopied the tumour-suppressing effects of miR-326 overexpression on melanoma cells. The restoration of the expression of KRAS markedly reversed the antitumour effects induced by miR-326 overexpression in melanoma cells. Further experiments indicated that miR-326 inactivated the AKT and ERK signalling pathways in melanoma. Collectively, these results revealed that miR-326 serves as a tumour suppressor in melanoma by targeting KRAS and regulating the AKT and ERK signalling pathways, indicating that miR-326 may be a promising therapeutic target for melanoma patients.

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Section: Discussionmentioning

confidence: 94%

“…Several miR-326 targets, including Bcl-2 (38) in osteosarcoma, FSCN1 (39) and NOB1 (41) in gastric cancer, SMO (47) and PKM2 (43) in glioma and CCND1 (25), phox2a (44), SP1 (45) and ADAM17 (46) in lung cancer, have been identified. In the present study, KRAS was validated as a novel target of miR-326.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-326 inhibits melanoma progression by targeting KRAS and suppressing the AKT and ERK signalling pathways

Kang

Zhang

et al. 2017

Oncol Rep

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“…In our study, we investigated the effect of EWSAT1 in NPC cell lines and discovered that EWSAT1 involved in the ceRNA regulatory network and functioned as endogenous miRNA sponges to bind to miR-326/330-5p and regulated its function. Recent studies indicated miR-326/330-5p showed tumor suppressive role on lung cancer [43–46], breast cancer [47], malignant melanoma [48], colorectal cancer [49], and glioblastoma [50,51], while their role on NPC had not been investigated. In our present study, miR-326/330-5p inhibited growth in NPC cell lines.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p

Song

Yin

2016

Aging

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Long non-coding RNA (lncRNA) Ewing sarcoma associated transcript 1 (EWSAT1) has been identified as an oncogene, and its dysregulation is closed corrected with tumor progression in Ewing sarcoma. Recently, high-through put analysis reveals that EWSAT1 is also highly expressed in human nasopharyngeal carcinoma (NPC). However, whether the aberrant expression of EWSAT1 in NPC is corrected with malignancy or prognosis has not been expounded. Herein, we identified that EWSAT1 was up-regulated in NPC tissues and cell lines, and higher expression of EWSAT1 resulted in a markedly poorer survival time. EWSAT1 over-expression facilitated, while EWSAT1 silencing impaired cell growth in NPC. In addition, mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive ‘sponge’ of miR-326/330-5p clusters. Collectively, our data revealed that EWSAT1 promotes NPC cell growth in vitro through up-regulating cyclin D1 partially via ‘spongeing’ miR-326/330-5p clusters.

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“…3)With the bridge factors，HOTAIR can achieve the regulation of chromatin region and gene expression by guiding the histone modifiers, such as PRC2. Moreover, HOTAIR repression reversed chemoresistance in LAD cells partially by regulating the miR-326/ SP1 pathways [33]. MiR-326 is regulated by HOTAIR and Phox2a, a vertebrate homeodomain transcription factor.…”

Section: Waf1/cip1mentioning

confidence: 94%

HOTAIR: An Oncogenic Long Non-Coding RNA in Human Cancer

Tang

Hann

2018

Cell Physiol Biochem

204

127

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Long non-coding RNAs (LncRNAs) represent a novel class of noncoding RNAs that are longer than 200 nucleotides without protein-coding potential and function as novel master regulators in various human diseases, including cancer. Accumulating evidence shows that lncRNAs are dysregulated and implicated in various aspects of cellular homeostasis, such as proliferation, apoptosis, mobility, invasion, metastasis, chromatin remodeling, gene transcription, and post-transcriptional processing. However, the mechanisms by which lncRNAs regulate various biological functions in human diseases have yet to be determined. HOX antisense intergenic RNA (HOTAIR) is a recently discovered lncRNA and plays a critical role in various areas of cancer, such as proliferation, survival, migration, drug resistance, and genomic stability. In this review, we briefly introduce the concept, identification, and biological functions of HOTAIR. We then describe the involvement of HOTAIR that has been associated with tumorigenesis, growth, invasion, cancer stem cell differentiation, metastasis, and drug resistance in cancer. We also discuss emerging insights into the role of HOTAIR as potential biomarkers and therapeutic targets for novel treatment paradigms in cancer.

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miR-326 reverses chemoresistance in human lung adenocarcinoma cells by targeting specificity protein 1

Cited by 47 publications

References 31 publications

MicroRNA-326 inhibits melanoma progression by targeting KRAS and suppressing the AKT and ERK signalling pathways

MicroRNA-326 inhibits melanoma progression by targeting KRAS and suppressing the AKT and ERK signalling pathways

Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p

HOTAIR: An Oncogenic Long Non-Coding RNA in Human Cancer

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