RETRACTED: Stress induced phosphoprotein 1 promotes tumor growth and metastasis of melanoma via modulating JAK2/STAT3 pathway

Sun, Xiaoyan; Cao, Ningjia; Mao, Liang; Cao, Wei

doi:10.1016/j.biopha.2019.108962

Cited by 13 publications

(12 citation statements)

References 29 publications

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“…Our results suggest that STIP1 can enhance the proliferative, adhesive, and migratory ability, inhibit the apoptosis, and accelerate the growth, of lung adenocarcinoma. This is consistent with the results reported for STIP1 in melanoma 22…”

Section: Discussionsupporting

confidence: 93%

“…In gastric cancer, STIP1 participates in the EMT process and increases the invasive and metastatic ability of gastric cancer cells by acting on its target genes, c-Myc and cyclinD1, through the Wnt/β-catenin signaling pathway 24. In melanoma, the elevated expression of STIP1 increases tumor metastasis by promoting cell proliferation and suppressing apoptosis through JAK2/STAT3 signaling 22. The results of our study indicate that STIP1 may induce proliferation and growth in lung adenocarcinoma by activating the JAK2/STAT3 signaling pathway and participating in EMT.…”

Section: Discussionmentioning

confidence: 99%

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STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway

Guo

Yan

Zhang

et al. 2019

CMAR

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PurposeRecent studies have shown that STIP1 is associated with proliferation and migration in numerous types of tumors; however, the role of STIP1 in lung adenocarcinoma is still poorly understood. Therefore, the aim of this study was to evaluate the role of STIP1 in lung adenocarcinoma, in vitro and in vivo.MethodsThe expression of STIP1 in lung adenocarcinoma was assessed by immunohistochemistry, RT-qPCR, and Western blot. The effects of STIP1 on the proliferation of lung adenocarcinoma cells were detected by the cell counting kit-8 assay; the effect of STIP1 on adhesion of lung adenocarcinoma cells was detected by Giemsa staining, while the cell scratch and Transwell assays were employed to examine the effect of STIP1 on the migratory ability of lung adenocarcinoma cells. Finally, apoptosis was evaluated by Hoechst staining and flow cytometry.ResultsThe expression level of STIP1 in lung adenocarcinoma tissue was significantly higher than that in adjacent normal tissue (P<0.05). Compared with that in nontransfected controls, cell proliferation, adhesion, and migration, as well as vimentin protein expression and levels of phosphorylated JAK2/STAT3, were significantly decreased (P<0.05) in A549 lung adenocarcinoma cells transfected with STIP1 shRNA, whereas E-cadherin protein expression and rates of apoptosis were significantly increased in these cells (P< 0.05).ConclusionElevated expression of STIP1 in lung adenocarcinoma may enhance the proliferative, adhesive, and migratory ability, and reduce the apoptosis of lung adenocarcinoma cells through the JAK2/STAT3 signaling pathway and epithelial-mesenchymal transition (EMT), thereby promoting the recurrence and metastatic potential of this cancer. The results indicate that STIP1 may be an effective therapeutic target for the treatment of lung adenocarcinoma.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway

Guo

Yan

Zhang

et al. 2019

CMAR

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“…STAT3 is commonly activated during MM progression and promotes metastasis [ 62 , 63 ]. Stress-induced phosphoprotein 1 (STIP1) is overexpressed in MM compared to benign nevi and normal skin, respectively [ 64 ]. STIP1 stimulates the expression of Janus kinase 2 (JAK2), which activates STAT3 ( Figure 1 ) [ 64 ].…”

Section: Mechanism Of Action Of Mir-21 In Melanoma and Melanoma Cementioning

confidence: 99%

“…Stress-induced phosphoprotein 1 (STIP1) is overexpressed in MM compared to benign nevi and normal skin, respectively [ 64 ]. STIP1 stimulates the expression of Janus kinase 2 (JAK2), which activates STAT3 ( Figure 1 ) [ 64 ]. STAT3 plays an important role in self-renewal of MM stem-like cells [ 65 ].…”

Section: Mechanism Of Action Of Mir-21 In Melanoma and Melanoma Cementioning

confidence: 99%

MicroRNA-21-Enriched Exosomes as Epigenetic Regulators in Melanomagenesis and Melanoma Progression: The Impact of Western Lifestyle Factors

Melnik

John

Carrera-Bastos

et al. 2020

Cancers

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DNA mutation-induced activation of RAS-BRAF-MEK-ERK signaling associated with intermittent or chronic ultraviolet (UV) irradiation cannot exclusively explain the excessive increase of malignant melanoma (MM) incidence since the 1950s. Malignant conversion of a melanocyte to an MM cell and metastatic MM is associated with a steady increase in microRNA-21 (miR-21). At the epigenetic level, miR-21 inhibits key tumor suppressors of the RAS-BRAF signaling pathway enhancing proliferation and MM progression. Increased MM cell levels of miR-21 either result from endogenous upregulation of melanocytic miR-21 expression or by uptake of miR-21-enriched exogenous exosomes. Based on epidemiological data and translational evidence, this review provides deeper insights into environmentally and metabolically induced exosomal miR-21 trafficking beyond UV-irradiation in melanomagenesis and MM progression. Sources of miR-21-enriched exosomes include UV-irradiated keratinocytes, adipocyte-derived exosomes in obesity, airway epithelium-derived exosomes generated by smoking and pollution, diet-related exosomes and inflammation-induced exosomes, which may synergistically increase the exosomal miR-21 burden of the melanocyte, the transformed MM cell and its tumor environment. Several therapeutic agents that suppress MM cell growth and proliferation attenuate miR-21 expression. These include miR-21 antagonists, metformin, kinase inhibitors, beta-blockers, vitamin D, and plant-derived bioactive compounds, which may represent new options for the prevention and treatment of MM.

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“…JAK2 is a principal member of the JAK2/STAT3 (signal transducer and activator of transcription) signaling, which is identified to be frequently overactivated and closely involved in the occurrence of many human cancers, including melanoma. [23][24][25] Activated JAK2 triggers STAT3 activation and nucleus translocation by inducing tyrosine phosphorylation, which then leads to transcription and translation of downstream genes. 26 Therefore, targeting JAK2 signaling is a potential anticancer strategy.…”

Section: Dovepressmentioning

confidence: 99%

Knockdown of Long Non-Coding RNA LOC100132707 Inhibits the Migration of Uveal Melanoma Cells via Silencing JAK2

Ying¹,

Yao²,

Zhang³

et al. 2020

OTT

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Background/Objective Although lots of long non-coding RNAs (lncRNAs) have been demonstrated to be involved in carcinogenesis, the functions of numerous of lncRNAs remain unknown. Bioinformatics online database showed that lncRNA LOC100132707 was highly expressed in metastatic melanoma tissues, and its expression predicted a lower overall survival rate in melanoma patients. However, LOC100132707 function in uveal melanoma (UM) progression still remains unclear. In the present study, we aimed to elucidate the role and molecular mechanisms underlying LOC100132707 in UM. Methods RT-PCR was used to detect the levels of LOC100132707 in UM cells. Cell migration, invasion and tumorigenesis were tested by using the transwell chamber assay and in vivo assay. Results LOC100132707 expression in metastatic UM cell line MM28 was significantly higher than that of the non-metastatic UM cell lines, MP38, MP46 and MP65, as well as the expressions of LOC100132707-related genes, including XRN1, PARP14, JAK2, DDX60, BUB1 and SAMD9L. LOC100132707 downregulation significantly repressed cell migration and invasion abilities, whereas overexpressing JAK2 rescued these effects. Consistently, upregulation of LOC100132707 induced significant increases in cell migration and invasion abilities via upregulating JAK2. In addition, silencing of LOC100132707 significantly repressed the in vivo tumor formation ability in UM cells. Conclusion This study reveals that silence of LOC100132707 represses the migration of UM via downregulating JAK2. The LOC100132707/JAK2 axis might serve as a potent target for the prevention and treatment of UM metastasis.

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RETRACTED: Stress induced phosphoprotein 1 promotes tumor growth and metastasis of melanoma via modulating JAK2/STAT3 pathway

Cited by 13 publications

References 29 publications

<p>STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway</p>

<p>STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway</p>

MicroRNA-21-Enriched Exosomes as Epigenetic Regulators in Melanomagenesis and Melanoma Progression: The Impact of Western Lifestyle Factors

<p>Knockdown of Long Non-Coding RNA LOC100132707 Inhibits the Migration of Uveal Melanoma Cells via Silencing JAK2</p>

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