Effects of PTEN on the proliferation and apoptosis of colorectal cancer cells via the phosphoinositol-3-kinase/Akt pathway

Sun, Yan; Tian, Hua; Wang, Lin

doi:10.3892/or.2015.3804

Cited by 45 publications

(38 citation statements)

References 41 publications

(36 reference statements)

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“…In contrast, the inhibition of miR‐92a can significantly decrease cell growth and induce apoptosis, which was assessed in a previous study . Correspondingly, a previous study found that up‐regulated PTEN suppressed colorectal cancer cell proliferation and induced apoptosis, which suggested that down‐regulation of PTEN may deliver opposite results . These aforementioned evidences and findings reveal the role of miR‐92a overexpression and PTEN silencing in cervical cancer cell function.…”

Section: Discussionmentioning

confidence: 67%

Retracted: MicroRNA‐92a promotes tumor growth and suppresses immune function through activation of MAPK/ERK signaling pathway by inhibiting PTEN in mice bearing U14 cervical cancer

Kang

et al. 2018

Cancer Medicine

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Cervical cancer is known as the possible outcome of genital infection, while the molecular mechanisms of initiation, development, and metastasis of cervical cancer have not yet been fully elucidated. Our study aims to investigate the effects of microRNA‐92a (miR‐92a) on tumor growth and immune function by targeting PTEN via the MAPK/ERK signaling pathway in tumor‐bearing mice. C57BL/6 female mice were used for tumor‐bearing mouse models and their tumor and adjacent normal tissues were collected, and normal cervical tissues were obtained from normal mice. Serum levels of tumor necrosis factor‐α (TNF‐α) and soluble interleukin‐2 receptor (sIL‐2R) were detected by ELISA. The cells were divided into the normal, blank, negative control (NC), miR‐92a mimic, miR‐92a inhibitor, siRNA‐PTEN, and miR‐92a inhibitor + siRNA‐PTEN groups. Dual‐luciferase reporter assay was adopted to determine the relationship between PTEN and miR‐92a. Expressions of miR‐92a, PTEN, TNF‐α, sIL‐2R, ERK1, and ERK2 were tested by RT‐qPCR and Western blotting. Cell proliferation was detected by cell count kit‐8 ( CCK‐8); cell cycle and apoptosis were detected by flow cytometry. Compared with the normal cervical tissues and adjacent normal tissues, the cervical cancer tissues exhibited increased expressions of miR‐92a, p‐ERK1/2, and serum levels of TNF‐α and sIL‐2R while decreased PTEN expression. PTEN was confirmed to be the target gene of miR‐92a. As compared with the blank and NC groups, expressions of miR‐92a, ERK1 and ERK2 increased, and expressions of PTEN decreased in the miR‐92a mimic group. The miR‐92a mimic group exhibited increased expression levels of TNF‐α and sIL‐2R, cell proliferation, and cell number in S phase but decreased cell apoptosis, and cell number in G0/G1 phase, while the miR‐92a inhibitor group followed opposite trends. miR‐92a promotes tumor growth and suppresses immune function by inhibiting PTEN via activation of the MAPK/ERK signaling pathway in mice bearing U14 cervical cancer.

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Section: Discussionmentioning

confidence: 67%

Retracted: MicroRNA‐92a promotes tumor growth and suppresses immune function through activation of MAPK/ERK signaling pathway by inhibiting PTEN in mice bearing U14 cervical cancer

Kang

et al. 2018

Cancer Medicine

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“…This pathway is known to play a key role in numerous cellular functions including proliferation, adhesion, angiogenesis, migration, invasion, and metabolism [40-42]. Further, loss of PTEN expression has been indicated to be significantly associated with advanced TNM stage, distant metastasis and poor prognosis in CRC [28, 29]. …”

Section: Discussionmentioning

confidence: 99%

“…The tumor suppressor PTEN has been shown to be frequently mutated in a large number of human cancers, including CRC [28]. It has been reported that PTEN may function as a dual specificity phosphatase and regulate cell growth, apoptosis, invasion and differentiation by negatively regulating the PI3K/AKT signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

“…According to recent reports, several significant targets of miR-21 associated with malignancy have been experimentally validated, such as PTEN [14-20], programmed cell death 4 (PDCD4) [21-23], reversion-inducing cysteine-rich protein with Kazal motifs (RECK) [24], forkhead box O1 (FOXO1) [25], RhoB [26] and Cdc25a [27], and these targets may exert different effects on tumorigenesis. Among them, the PTEN protein was reported to be frequently silenced in CRC, and it has been shown to suppress tumor formation by inhibiting the PI3K/AKT pathway [28, 29]. Therefore, miR-21 might act as an important oncogene by regulating PTEN as one of its several target genes and thus may be a useful biomarker for the diagnosis and treatment in CRC.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-21 (Mir-21) Promotes Cell Growth and Invasion by Repressing Tumor Suppressor PTEN in Colorectal Cancer

Wu¹,

Song²,

Xiong³

et al. 2017

Cell Physiol Biochem

167

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Background/Aims: MicroRNA-21 (miR-21) has been demonstrated to play an important role in carcinogenesis; however, its mechanism of action in colorectal cancer (CRC) has not been fully elucidated. The aim of the present study was to explore the oncogenic function of miR-21 and its molecular mechanism in CRC. Methods: A total of 105 paired tumor and tumor-adjacent normal tissue specimens from CRC patients and two CRC cell lines (HCT-116 and SW480) were studied. The protein and mRNA expression levels of PTEN and miR-21 were examined using western blot analysis and real-time reverse transcription-PCR (qRT-PCR). Furthermore, we transfected CRC cells with different combinations of ectopic-expression vector or shRNA expression vector of miR-21 and phosphatase and tensin homolog (PTEN) to modulate the expression levels of miR-21 and PTEN respectively, and then analyzed the phenotypic alterations of CRC cells. Tumorigenesis was also evaluated by xenografting HCT-116 cells into nude mice. Results: In this study, we showed that miR-21 expression was significantly up-regulated in CRC compared to that in normal tissues. Patients with advanced Tumor-Node-Metastasis (TNM) stage, lymph node metastasis, local invasion and higher serum carcinoembryonic antigen (CEA) levels displayed significantly high expression of miR-21. The PTEN protein level in CRC tissues and cells was inversely correlated with miR-21 expression. Furthermore, the transfection of CRC cells with pre-miR-21 could inhibit apoptosis and promote cellular proliferation, invasion, cell cycle progression and growth of xenografts in nude mice, whereas the transfection of miR-21-specific shRNA resulted in the opposite phenomena. In addition, silencing or elevating PTEN protein could partially reverse the effect of miR-21-specific shRNA or pre-miR-21 on apoptosis, cell cycle distribution, and invasion of CRC cells. Moreover, over-expression or knockdown of miR-21 altered the protein expression of PTEN and phosphorylated Akt (p-AKT). Conclusion: miR-21 can modulate the malignant phenotypes such as proliferation, anti-apoptosis, cell cycle progression and invasion of CRC cells by down-regulating PTEN protein expression. The results of study might improve our understanding of the regulatory mechanism of miR-21 and provide useful targets and approaches for the clinical diagnosis and therapy of CRC.

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“…Phosphatase and tensin homolog (PTEN) inhibits phosphoinositide‐3‐kinase pathway by dephosphorylating PIP3 and prevents Akt activation [5]. Loss of PTEN in B cells of IgAN was evident in the array analysis conducted by Cox et al [6], and decrease of PTEN has been found to be related to cell proliferation in various diseases [7,8].…”

Section: Introductionmentioning

confidence: 99%

Increased miR‐374b promotes cell proliferation and the production of aberrant glycosylated IgA1 in B cells of IgA nephropathy

Zhou

Bao

et al. 2015

FEBS Letters

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a b s t r a c tThe number of B cells is increased and the O-glycans of IgA1 are incompletely galactosylated in IgA nephropathy (IgAN). Here we report that expression of phosphatase and tensin homolog (PTEN) and Cosmc is decreased in B cells, and correlates with B cell number and the aberrant glycosylation of IgA1 in IgAN. Patients with IgAN exhibit higher miR-374b in B cells compared to controls. We show that miR-374b targets PTEN and Cosmc by luciferase assays and western blot analysis. Inhibition of miR-374b increased PTEN and Cosmc expression, and prevented cell proliferation and aberrant glycosylation of IgA1, thus representing a new therapeutic approach for IgAN.

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Effects of PTEN on the proliferation and apoptosis of colorectal cancer cells via the phosphoinositol-3-kinase/Akt pathway

Cited by 45 publications

References 41 publications

Retracted: MicroRNA‐92a promotes tumor growth and suppresses immune function through activation of MAPK/ERK signaling pathway by inhibiting PTEN in mice bearing U14 cervical cancer

Retracted: MicroRNA‐92a promotes tumor growth and suppresses immune function through activation of MAPK/ERK signaling pathway by inhibiting PTEN in mice bearing U14 cervical cancer

MicroRNA-21 (Mir-21) Promotes Cell Growth and Invasion by Repressing Tumor Suppressor PTEN in Colorectal Cancer

Increased miR‐374b promotes cell proliferation and the production of aberrant glycosylated IgA1 in B cells of IgA nephropathy

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