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Last month, the artist and businesswoman Jane Zhang of Shanghai, a Seattle native, created a surprise party for herself and paid for it with the $4.5 million she had raised after her Instagram account was flooded with adoration. At 23, she is the youngest entrepreneur to have a company valued at $1 billion, the youngest one to earn an MBA from Harvard, the youngest to be named one of TIME’s 100 most influential people in the world and, in 2016, one of China’s richest women.
And yet, at the party, Ms. Zhang was mobbed by fans who followed her on her big Instagram photos. Despite signs at the entrance notifying guests they would be photographed only if they wanted to, she stopped off at a photographer’s space and posed for some of the party’s most high-profile guests, including actress Jennifer Lawrence, designer Andrew Gn and singers Iggy Azalea and Zendaya.
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Ms. Zhang was the earliest teen candidate for membership in the exclusive Forbes 400, and she is to postgraduates what Justin Bieber is to 10-year-olds: both formidable and vulnerable.
At the party, her warmth shone through, especially when she sent a group of eager fans, known as “Zhang Gang,” to find Chinese snacks and drinks for guests. At one point, she recognized a college buddy who had graduated from Georgetown, La Salle, Boston College and Cornell.
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Though she was born to entrepreneurs, Ms. Zhang grew up in the suburbs of Seattle, in a seemingly ordinary family. Her father, Tuyu, was in real estate, and her mother, Xiao Min Zhang, taught in a public school. Her parents divorced when she was 6 and she recalls long flights to Seattle with her mother, who had few possessions.
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Breast cancer is one of the most common cancer in women. Recently, lncRNAs were revealed to play important roles in the growth, progression, metastasis and the drug resistance in many types of cancers. However, the role of long non-coding RNA breast cancer related 1 (BNCR1) in breast cancer remains unknown. In this study, we reported that BNCR1 was up-regulated in breast cancer and high expression of BNCR1 was a bad prognosis factor. Overexpression of BNCR1 promoted cell proliferation, colony formation, migration and invasion of breast cancer cells. In contrast, knockdown of BNCR1 inhibited cell proliferation, colony formation, migration and invasion of breast cancer cells. Moreover, BNCR1 promoted cell cycle progression and up-regulated expression of Cyclin D1, CDK2, CDK4 and Cyclin E1. The results showed that BNCR1 can function as a molecular sponge for miR-138, and miR-138 targeted Cyclin D1 and CDK4. Furthermore, miR-138 overexpression abrogated the cell proliferation, colony formation, migration and invasion of breast cancer cells promoted by BNCR1. Taken together, our data suggested that BNCR1 may be a oncogene in breast cancer and miR-138 overexpression may inhibit cell growth, colony formation, migration and invasion of breast cancer cells through targeting Cyclin D1 and CDK4.Q:
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