Editorial Comment from Dr Namekawa to Differences in semen characteristics between patients with testicular cancer and other malignancies using various cut‐off values

Namekawa, Takeshi

doi:10.1111/iju.13765

Cited by 1 publication

(1 citation statement)

References 5 publications

(10 reference statements)

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“…‘Individualized treatment’ has become the new guiding principle for clinical work, but approximately 30% of breast cancer patients will still have recurrence and metastasis after comprehensive systemic treatment [18]. In some breast cancer patients who have already metastasized at the time of initial diagnoses, traditional chemotherapeutic drugs have obvious effects at first, but most patients will relapse and become resistant after a period of time [19]. Although the use of chemical drugs can significantly improve the survival rate of breast cancer patients, 80% of patients will develop resistance to varying degrees [20].…”

Section: Discussionmentioning

confidence: 99%

miR-221/222 promote tumor growth and suppress apoptosis by targeting lncRNA GAS5 in breast cancer

et al. 2019

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MicroRNAs (miRNAs) are 21–23-nucleotide, short, non-coding RNAs that play important roles in virtually all biological pathways in mammals and other multicellular organisms. The association of miR-221 and miR-222 (miR-221/222) for breast cancer is critical, but their detailed roles in its development and progression remain unclear. In the present study, we found that miR-221/222 were consistently up-regulated in breast cancer tissues. We then investigated the molecular mechanisms by which miR-221/222 contributed to breast cancer and identified growth arrest–specific transcript 5 (GAS5) as a direct target gene of miR-221/222. In contrast with the up-regulated expression levels of miR-221/222, GAS5 levels were significantly down-regulated and negatively correlated with miR-221/222 in breast cancer tissues. In addition, we showed that miR-221/222 inhibitors increased cellular apoptosis, miR-221/222 mimics decreased the cell apoptosis in breast cancer cells, and restoration of GAS5 expression attenuated the anti-apoptotic effects of miR-221/222 in breast cancer cells, indicating that GAS5 was a direct mediator of miR-221/222 function. Finally, we showed that miR-221/222 suppressed GAS5 expression significantly and enhanced tumor growth in a mouse model of breast cancer xenografts. The present study highlighted the important role of miR-221/222 as oncomiRs in breast cancer, which inhibited GAS5 translation. These findings may provide a new perspective for the molecular mechanism of breast carcinogenesis and provide a novel approach to the treatment of breast cancer.

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Section: Discussionmentioning

confidence: 99%