Long non-coding RNA UCA1 enhances drug resistance of lung cancer cells via activating mTOR signaling

There is accumulating evidence suggesting that long non-coding RNA (lncRNA) UCA1 is involved in the resistance of the tumor to chemotherapeutic agents. Enhanced expression of UCA1 is frequently observed in patients with lung cancer. However, the role of UCA1 in regulating chemoresistance of lung cancer cells remains largely unknown. Here we reported that overexpression of UCA1 significantly enhanced the resistance of lung cancer cells to rapamycin. Overexpression of UCA1 enhanced mTOR phosphorylation and potently reduced rapamycin-induced inhibition of mTOR signaling, resulting in enhanced viability of A549 cells upon rapamycin treatment. Consistently, knockdown of mTOR largely abolished UCA1-mediated resistance to rapamycin treatment. In addition, we showed that A549 sphere was characterized by enhanced expression of UCA1, high activity of mTOR signaling as well as elevated resistance to rapamycin treatment. Together, these results indicated that UCA1 could enhance chemoresistance of lung cancer cells via activating mTOR signaling, suggesting a role of UCA1 as a new effective therapeutic target for lung cancer treatment.