The incidence and death rate of colorectal cancer ( CRC ) is very high, which brings great need to understand the early molecular events of CRC . These studies demonstrate that long noncoding RNA (lnc RNA ) plays an important role in the occurrence and development of human cancer. Small nucleolar RNA host gene 15 ( SNHG 15) was recently identified as a cancer‐related lnc RNA . In this study, we aimed to evaluate the function and mechanism of SNHG 15 in CRC . The expression of SNHG 15 was detected by quantitative RT ‐ PCR ( qRT ‐ PCR ) in CRC tissues and matched noncancerous tissues ( NCT s). CCK ‐8 assay, colony formation assay, flow cytometric analysis, and nude mouse xenograft mode were used to examine the tumor‐promoting function of SNHG 15 in vitro and in vivo. The binding relationship between SNHG 15, miR‐338‐3p and the target genes of miR‐338‐3p were screened and identified by databases, qRT ‐ PCR , dual luciferase reporter assay and western blot. Our results showed that SNHG 15 was up‐regulated in CRC tissues compared with paired NCT s ( P < 0.0001). High level of SNHG 15 expression predicted poor prognosis of CRC ( P = 0.0051). SNHG 15 overexpression could promote cell proliferation and inhibit cell apoptosis. Animal experiments showed that up‐regulation of SNHG 15 promoted tumor growth in vivo. The results of mechanism experiments showed that SNHG 15 could bind to miR‐338‐3p and block its inhibition on the expression and activity of FOS or RAB 14. In conclusion SNHG 15 promotes cell proliferation through SNHG 15/miR‐338‐3p/ FOS ‐ RAB 14 axis in CRC.

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Piperlongumine (PL), a natural alkaloid present in the fruit of the Long pepper, is known to exhibit notable anti-cancer effects. Nonetheless, the anti-tumor effect of PL in lung cancer cells still remains unclear. In the present study, we reported the chemotherapeutic effects of PL using in vitro and in vivo models. We showed that PL displayed potent anti-neoplastic activity against lung cancer A549 cells as well as corresponding docetaxel-resistant A549/DTX cells. In addition, we found that PL induced apoptosis in both A549 and A549/DTX cells. PL also induced autophagy in A549/DTX cells. Moreover, autophagy-specific inhibitors (3-methyladenine) or Beclin1 and Atg 5 small interfering RNAs (siRNAs) enhanced PL-induced apoptosis, indicating that PL-mediated autophagy may protect A549/DTX cells from undergoing apoptotic cell death. Furthermore, we observed the inhibition of phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway by PL. Finally, PL inhibited the growth of A549/DTX xenograft tumors, which was associated with inhibition of cell proliferation, induction of apoptosis of tumor cells and decreased expression of p-Akt and p-mTOR in tumor xenograft tissues. In summary, our study demonstrated that PL induced apoptosis and autophagy through modulation of the PI3K/Akt/mTOR pathway in human lung cancer cells. This study may provide a rationale for future clinical application using PL as a chemotherapeutic agent for lung cancer.