MicroRNA-150 promotes cell proliferation, migration, and invasion of cervical cancer through targeting PDCD4

Zhang, Zhan; Wang, Jinming; Li, Jing; Wang, Xiaofang; Song, Wanyu

doi:10.1016/j.biopha.2017.09.143

Cited by 63 publications

(45 citation statements)

References 21 publications

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“…GC accounts for 10% of all diagnosed cancer types each year and accounts for 12% of all cancer associated mortalities worldwide (2,4). It is also one of the most common malignancies (13,14). The current study assessed the role and mechanism of miR-150-SRCIN1 in the pathogenesis of GC development.…”

Section: Discussionmentioning

confidence: 99%

“…The abnormal expression of miRNA is associated with a variety of diseases including tumors (7). miRNA has been demonstrated to be involved in the regulation of tumor cell proliferation, apoptosis, differentiation, drug resistance, invasion and metastasis, among which miR-150 also ion, drug resistance, invasion and metastasis, among which miR-150 also serves an important role in the development of tumors (10)(11)(12)(13)(14)(15). In colorectal cancer, breast cancer and melanoma, miR-150 is significantly downregulated and exerts a tumor suppressive role (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

“…In colorectal cancer, breast cancer and melanoma, miR-150 is significantly downregulated and exerts a tumor suppressive role (11)(12)(13). However, in cervical cancer, miR-150 is highly expressed and promotes tumor progression (14). Therefore, miR-150 serves different roles in different tumor types (10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

“…However, in cervical cancer, miR-150 is highly expressed and promotes tumor progression (14). Therefore, miR-150 serves different roles in different tumor types (10)(11)(12)(13)(14). miR-150-5p, a member of the miR-150 family, has been determined to inhibit cancer cell aggressiveness by targeting cwcv and kazal like domains proteoglycan 1 in head and neck squamous cell carcinoma (15).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑150‑5p and SRC kinase signaling inhibitor 1 involvement in the pathological development of gastric cancer

Quan

Chen

et al. 2019

Exp Ther Med

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The current study aimed to assess the regulatory mechanism of microRNA-150-5p (miR-150-5p) in the pathogenesis of gastric cancer. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to verify the expression of miR-150-5p in gastric cancer tissues and cell lines, which was revealed to be highly expressed in each. In addition, the expression of miR-150-5p was associated with advanced gastric cancer and lymph node metastasis. The current study then hypothesized that SRC kinase signaling inhibitor 1 (SRCIN1) was the target gene of miR-150-5p, a theory that was confirmed via a dual luciferase reporter gene assay. RT-qPCR and western blotting were then performed to verify the expression of SRCIN1 in gastric cancer tissues and cell lines. The results demonstrated that SRCIN1 was lowly expressed in gastric cancer tissues and cells. To assess the effect of miR-150-5p on gastric cancer cells, experiments were conducted with BGC-823 cells transfected with a miR-150-5p inhibitor or a miR-150-5p inhibitor+SRCIN1-small interfering (si)RNA respectively. A cell counting kit-8 assay and flow cytometry were also used to assess cell viability and apoptosis, respectively. Western blotting and RT-qPCR were further used to measure the expression of specific markers of epithelial mesenchymal transition (EMT), including epithelial cell markers (E-cadherin and zona occluding-1) and interstitial cell markers (vimentin, N-cadherin and β-catenin). The results revealed that the miR-150-5p inhibitor attenuated cell viability, induced apoptosis, decreased the expression of interstitial cell markers and increased epithelial cell marker expression. However, all effects of the miR-150-5p inhibitor were reversed following SRCIN1-siRNA treatment. In summary, the current study indicated that the miR-150-5p inhibitor attenuated cell viability, induced apoptosis and inhibited gastric cancer cell EMT by targeting SRCIN1.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑150‑5p and SRC kinase signaling inhibitor 1 involvement in the pathological development of gastric cancer

Quan

Chen

et al. 2019

Exp Ther Med

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“…Programmed cell-death factor 4 (PDCD4) is an apoptosis-associated gene (6) and is downregulated in many malignant tumors, including CRC (7)(8)(9)(10)(11)(12). Its loss or downregulated expression has been found to promote tumor cell proliferation, invasion and metastasis, and to reduce tumor cell apoptosis in multiple cancer types, including cervical cancer (7), non-small cell lung cancer (NSCLC) (8), breast cancer (9), CRC (11)(12)(13)(14)(15), gastric cancer (10,16), and esophageal squamous cell carcinoma (17), among others. Furthermore, loss or reduced PDCD4 expression has been reported to be associated with tumor progression and poor prognosis in CRC (11,12), NSCLC (8,18) and other malignant cancers.…”

Section: Introductionmentioning

confidence: 99%

Programmed cell death factor 4 enhances the chemosensitivity of colorectal cancer cells to Taxol

et al. 2019

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Drug resistance and disease relapse are still challenging problems in the chemotherapy of colorectal cancer (CRC). Programmed cell death factor 4 (PDCD4) has previously been reported to act as a tumor suppressor and was implicated in the chemosensitivity of numerous types of human malignancy. In this study, the effect of PDCD4 in the sensitivity of CRC to the chemotherapy drug Taxol was investigated. The results confirmed that lower PDCD4 expression was present in CRC tumor tissues, when compared with in normal adjacent tissues (p) and closely associated with the prognosis of patients with CRC. Upregulation of PDCD4 significantly enhanced the sensitivity of CRC cells to Taxol, by partially contributing to pro-apoptosis and anti-invasion pathways, both through upregulation of the apoptosis-associated protein Bax, and downregulation of the anti-apoptosis protein Bcl-2 and invasion-associated proteins MMP-9. These findings might present a novel strategy for sensitizing tumor cells to apoptosis and, thus, overcoming chemotherapy resistance in CRC.

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Programmed cell death 4: A novel player in the pathogenesis of polycystic ovary syndrome

Zarezadeh,

Abbasi,

Aboutalebi Vand Beilankouhi

et al. 2023

Cell Biochemistry & Function

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Polycystic ovary syndrome (PCOS) is a pathological condition recognized by menstrual cycle irregularities, androgen excess, and polycystic ovarian morphology, affecting a significant proportion of women of childbearing age and accounting for the most prevalent cause of anovulatory sterility. In addition, PCOS is frequently accompanied by metabolic and endocrine disturbances such as obesity, dyslipidemia, insulin resistance, and hyperinsulinemia, indicating the multiplicity of mechanisms implicated in the progression of PCOS. However, the exact pathogenesis of PCOS is yet to be elucidated. Programmed cell death 4 (PDCD4) is a ubiquitously expressed protein that contributes to the regulation of various cellular processes, including gene expression, cell cycle progression, proliferation, and apoptosis. Despite some disparities concerning its exact cellular effects, PDCD4 is generally characterized as a protein that inhibits cell cycle progression and proliferation and instead drives the cell into apoptosis. The apoptosis of granulosa cells (GCs) is speculated to take a major part in the occurrence and progression of PCOS by ceasing antral follicle development and compromising oocyte competence. Given the possible involvement of GC apoptosis in the progression of PCOS, as well as the contribution of PDCD4 to the regulation of cell apoptosis and the development of metabolic diseases, the current review aimed to discuss whether or how PDCD4 can play a role in the pathogenesis of PCOS by affecting GC apoptosis.

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MicroRNA-150 promotes cell proliferation, migration, and invasion of cervical cancer through targeting PDCD4

Cited by 63 publications

References 21 publications

MicroRNA‑150‑5p and SRC kinase signaling inhibitor 1 involvement in the pathological development of gastric cancer

MicroRNA‑150‑5p and SRC kinase signaling inhibitor 1 involvement in the pathological development of gastric cancer

Programmed cell death factor 4 enhances the chemosensitivity of colorectal cancer cells to Taxol

Programmed cell death 4: A novel player in the pathogenesis of polycystic ovary syndrome

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