miR-106a confers cisplatin resistance by regulating PTEN/Akt pathway in gastric cancer cells

Fang, Yue; Shen, Huiling; Li, Hao; Cao, Yuan; Qin, Rong; Long, Lingliang; Zhu, Xiaolan; Xie, Changqing; Xu, Wenlin

doi:10.1093/abbs/gmt106

Cited by 63 publications

(51 citation statements)

References 34 publications

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“…Similarly, treatment of gastric cancer cells with PI3K inhibitor abrogated miR-106a induced activation of Akt and led to the considerable suppression of miR-106a mediated cell survival and cisplatin resistance. Generally, this study confirms that miR-106a confers cell survival and cisplatin resistance through regulation of PI3K/Akt pathway in human gastric cancer via targeting PTEN and may be utilized as a novel therapeutic target in the treatment of gastric cancer [87].…”

Section: 223supporting

confidence: 76%

“…miR-106a is upregulated in gastric tumors and promotes tumor growth [29]. A recent study examined the contribution of miR-106a dysregulation to the development of cisplatin (DDP) resistance in gastric cancer cell lines [87]. They found that miR-106a was significantly overexpressed in cisplatin resistant gastric cancer cells SGC7901/DDP when compared with their parental cells SGC7901, suggesting that elevated miR-106a levels could be correlated with cisplatin resistance in gastric cancer cells.…”

Section: 223mentioning

confidence: 99%

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MicroRNA-induced drug resistance in gastric cancer

Dehghanzadeh

Jadidi‐Niaragh

Gharibi

et al. 2015

Biomedicine & Pharmacotherapy

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Section: 223supporting

confidence: 76%

Section: 223mentioning

confidence: 99%

MicroRNA-induced drug resistance in gastric cancer

Dehghanzadeh

Jadidi‐Niaragh

Gharibi

et al. 2015

Biomedicine & Pharmacotherapy

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“…In the present study, we identified the deregulation of miR-106a in ovarian cancer. miR-106a is widely expressed in diverse human tumors, including gastric, non-small cell lung, pancreatic, colorectal and ovarian cancer (6,8,9,(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53). Previous studies showed that miR-106a acts as a tumor suppressor or an oncogene in different cancers, depending on the different cellular context.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

et al. 2016

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Abstract. Ovarian cancer is a leading cause of malignant gynecological tumor-related mortality among women. The treatment of ovarian cancer patients continues to be challenging. MicroRNA-106a (miR-106a) is widely expressed in diverse human tumors. In the present study, we investigated the biological and pathological roles of miR-106a in ovarian cancers. We found that miR-106a expression was significantly increased in primary ovarian cancer tissues and ovarian cancer cells compared with the level in normal tissues. Ectopic expression of an miR-106a inhibitor attenuated ovarian cancer cell proliferation and invasion. miR-106a promoted the growth and invasion of SKOV3 cells by targeting phosphatase and tensin homolog (PTEN). Furthermore, the present study revealed that IL-6 inhibited miR-106a expression by activating STAT3. Tocilizumab, a humanized anti-human IL-6R antibody, that competitively inhibits IL-6/IL-6R signaling, did not inhibit the proliferation and invasion of SKOV3 cells. In conclusion, our studies revealed that miR-106a was significantly increased in the ovarian cancer tissues and cell lines. Downregulation of the expression of miR-106a inhibited cell growth and metastasis of ovarian cancer cells. Together, the present study suggests that miR-106a acts as an oncogene in ovarian cancers.

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“…MiR-106a-3p, which belongs to the miR-17 family, is involved in many types of tumors [62], [63], [64]; additionally, miR-106a directly regulates Stat3 [65] and IL-10 [66]. Stat3 is the signal transducer for IFN-γ in some cell types [23], whereas IL-10 inhibits IFN-γ production through inhibition of IL-12 [67], [68].…”

Section: Discussionmentioning

confidence: 99%

Differential Expression Profiling of Spleen MicroRNAs in Response to Two Distinct Type II Interferons in Tetraodon nigroviridis

Wan

et al. 2014

PLoS ONE

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MicroRNAs are endogenous, small non-coding RNAs approximately 18–26 nucleotides in length that regulate target gene expression at the post-transcription level. Interferon-γ (IFN-γ) is a Th1 cytokine that is involved in both the innate and adaptive immune responses. We previously identified two IFN-γ genes in green-spotted puffer fish (Tetraodon nigroviridis). To determine whether miRNAs participate in IFN-γ-related immune responses, T. nigroviridis spleen cells were treated with recombinant IFN-γ isoforms, and a Solexa high-throughput sequencing method was used to identify miRNAs. In total, 1,556, 1,538 and 1,573 miRNAs were found in the three samples, and differentially expressed miRNAs were determined. In total, 398 miRNAs were differentially expressed after rIFN-γ1 treatment, and 438 miRNAs were differentially expressed after rIFN-γ2 treatment; additionally, 403 miRNAs were differentially expressed between the treatment groups. Ten differentially expressed miRNAs were chosen for validation using qRT-PCR. Target genes for the differentially expressed miRNAs were predicted, and GO and KEGG analyses were performed. This study provides basic knowledge regarding fish IFN-γ-induced miRNAs and offers clues for further studies into the mechanisms underlying fish IFN-γ-mediated immune responses.

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miR-106a confers cisplatin resistance by regulating PTEN/Akt pathway in gastric cancer cells

Cited by 63 publications

References 34 publications

MicroRNA-induced drug resistance in gastric cancer

MicroRNA-induced drug resistance in gastric cancer

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

Differential Expression Profiling of Spleen MicroRNAs in Response to Two Distinct Type II Interferons in Tetraodon nigroviridis

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