Ginsenoside Rh2 inhibits prostate cancer cell growth through suppression of micro<scp>RNA</scp>‐4295 that activates <scp>CDKN</scp>1A

Gao, Qiruo; Zheng, Junhua

doi:10.1111/cpr.12438

Cited by 51 publications

(31 citation statements)

References 32 publications

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“…Chemotherapy drugs are currently the preferred treatment for patients with CRPC. However, these prostate cancers will always become dually resistant against both the ADT and chemotherapy drugs in just a few months (1,(14)(15)(16), which can have adverse effects on the patient's survival. Thus, new treatments for refractory prostate cancer are urgently needed.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Inhibitor 9 Combined With Androgen Deprivation Therapy or Chemotherapy Delays the Malignant Behavior of Castration-Resistant Prostate Cancer Through K-Ras/PLCε/PKCε Signaling Pathway

et al. 2020

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Castration-resistant prostate cancer (CRPC) is a progressed stage of prostate cancer, which requires better understanding of the mechanisms and remains an unmet clinical need. As a common oncogene, K-Ras is associated with malignant behavior in different types of tumors but its role in CRPC is unknown. The present study aims to find the mechanism of K-Ras in CRPC and whether it can be used as a crucial molecule for the treatment of CRPC. For this purpose, tissue samples from primary prostate cancer (PPC) and CRPC patients were analyzed by immunohistochemistry and the data showed that K-Ras was elevated in CRPC. More importantly, higher K-Ras expression was related to a shorter recurrence-free survival time in patients with CRPC. In addition, K-Ras promoted the invasion, migration, and drug resistance of CRPC cells by activation of PLCε/PKCε signaling pathway. Meanwhile, the inhibitor of K-RasG12C mutants was able to inhibit malignant behavior of CRPC cells in vitro and in vivo. Inhibitors of K-RasG12C mutants have entered clinical trials. Taken together, the study shows that K-Ras may activate PKCε through PLCε, resulting in the alterations of malignant behavior of CRPC. Inhibitor 9, an inhibitor of the K-RasG12C mutant, has a strong anti-tumor effect in CRPC, which potentially suggests that inhibitors of this nature may serve as a promising treatment for CRPC.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Inhibitor 9 Combined With Androgen Deprivation Therapy or Chemotherapy Delays the Malignant Behavior of Castration-Resistant Prostate Cancer Through K-Ras/PLCε/PKCε Signaling Pathway

et al. 2020

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“…Concerning PCa, genistein has shown promise in modulating the levels of different oncogenic (i.e., miR221, miR222, miR151, and miR1260b) and oncosuppressor (i.e., miR-574-3p and miR34a) miRNAs, thus affecting cancer cell proliferation [115][116][117][118][119][120]. Similar encouraging data were also obtained from in vitro studies with luteolin, curcumin, resveratrol, ginsenoside Rh2, and celastrol [121][122][123][124][125][126].…”

Section: Natural Compounds Affecting Proliferationmentioning

confidence: 63%

Natural Compounds in Prostate Cancer Prevention and Treatment: Mechanisms of Action and Molecular Targets

Fontana

Raimondi

Marzagalli

et al. 2020

Cells

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Prostate cancer (PCa) represents a major cause of cancer mortality among men in developed countries. Patients with recurrent disease initially respond to androgen-deprivation therapy, but the tumor eventually progresses into castration-resistant PCa; in this condition, tumor cells acquire the ability to escape cell death and develop resistance to current therapies. Thus, new therapeutic approaches for PCa management are urgently needed. In this setting, natural products have been extensively studied for their anti-PCa activities, such as tumor growth suppression, cell death induction, and inhibition of metastasis and angiogenesis. Additionally, numerous studies have shown that phytochemicals can specifically target the androgen receptor (AR) signaling, as well as the PCa stem cells (PCSCs). Interestingly, many clinical trials have been conducted to test the efficacy of nutraceuticals in human subjects, and they have partially confirmed the promising results obtained in vitro and in preclinical models. This article summarizes the anti-cancer mechanisms and therapeutic potentials of different natural compounds in the context of PCa prevention and treatment.

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“…The transfected cell samples of SCC-4 and SCC-9 were washed employing PBS and fixed using 4% PFS for TUNEL assay [ 19 ], in the presence of TUNEL assay reagent (Merck KGaA, Darmstadt, Germany). Following addition of DAPI staining solution, cell samples were analyzed using optical microscopy (Olympus).…”

Section: Methodsmentioning

confidence: 99%

LncRNA TTN-AS1 promotes the progression of oral squamous cell carcinoma via miR-411-3p/NFAT5 axis

Zhang

Shen

et al. 2020

Cancer Cell Int

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Background: Oral squamous cell carcinoma (OSCC) is a common kind of squamous cell carcinoma of the head and neck, which is a threat to public health. Long noncoding RNAs (lncRNAs) are associated with the development of various diseases, including cancers. LncRNA titin antisense RNA 1 (TTN-AS1) is known as a crucial regulatory factor in several cancers. Nevertheless, the specific functions of TTN-AS1 in OSCC remains obscure. Methods: The expression of TTN-AS1 in OSCC samples or cells was analyzed through qRT-PCR. Colony formation assay, EdU assay, flow cytometry assay, TUNEL assay and wound healing assay were conducted to estimate the functions of TTN-AS1 in OSCC cells. RIP and luciferase reporter assays were utilized to detect the interaction between TTN-AS1 and miR-411-3p as well as between miR-411-3p and NFAT5. Results: TTN-AS1 expression was stronger in OSCC cells. Knockdown of TTN-AS1 effectively restrained cell proliferation and migration but had inductive role in apoptosis. Moreover, TTN-AS1 could function as the miR-411-3p sponge in OSCC and miR-411-3p exerted the inhibitory functions on OSCC cell growth. In addition, NFAT5 was proven as the target of miR-411-3p. Rescue assay indicated that overexpressing NFAT5 could reverse the inhibitory function of TTN-AS1 depletion on cell growth. Conclusion: lncRNA TTN-AS1 contributed to the progression of OSCC via miR-411-3p/NFAT5 axis.

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Ginsenoside Rh2 inhibits prostate cancer cell growth through suppression of microRNA‐4295 that activates CDKN1A

Abstract: GRh2 may inhibit PC cell growth through suppression of microRNA-4295 that activates CDKN1A.

Cited by 51 publications

References 32 publications

RETRACTED: Inhibitor 9 Combined With Androgen Deprivation Therapy or Chemotherapy Delays the Malignant Behavior of Castration-Resistant Prostate Cancer Through K-Ras/PLCε/PKCε Signaling Pathway

RETRACTED: Inhibitor 9 Combined With Androgen Deprivation Therapy or Chemotherapy Delays the Malignant Behavior of Castration-Resistant Prostate Cancer Through K-Ras/PLCε/PKCε Signaling Pathway

Natural Compounds in Prostate Cancer Prevention and Treatment: Mechanisms of Action and Molecular Targets

LncRNA TTN-AS1 promotes the progression of oral squamous cell carcinoma via miR-411-3p/NFAT5 axis

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