Colorectal Cancer (CRC) is one of the most common digestive system malignant tumors.
Recently, PDT has been used as a first-line treatment for colon cancer; however, limited
curative effect was obtained due to resistance of CRC to PDT. During the past decades,
accumulating CRC-related long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and mRNAs
have been reported to exert diverse functions through various biological processes;
their dysregulation might trigger and/or promote the pathological changes. Herein,
we performed microarrays analysis to identify dysregulated lncRNAs, miRNAs and mRNAs
in PDT-treated HCT116 cells to figure out the lncRNA-miRNA interactions related to
the resistance of CRC to PDT treatment, and the downstream mRNA target, as well as
the molecular mechanism. We found a total of 1096 lncRNAs dysregulated in PDT-treated
CRC HCT116 cells; among them, LIFR-AS1 negatively interacted with miR-29a, one of
the dysregulated miRNAs in PDT-treated CRC cells, to affect the resistance of CRC
to PDT. LIFR-AS1 knockdown attenuated, whereas miR-29a inhibition enhanced the cellular
effect of PDT on HCT116 cell proliferation and apoptosis. Furthermore, among the dysregulated
mRNAs, TNFAIP3 was confirmed to be a direct target of miR-29a and exerted a similar
effect to LIFR-AS1 on the cellular effects of PDT. In summary, LIFR-AS1 serves as
a competitive endogenous RNA (ceRNA) for miR-29a to inhibit its expression and up-regulate
downstream target TNFAIP3 expression, finally modulating the resistance of CRC to
PDT. We provide an experimental basis for this lncRNA/miRNA/mRNA network being a promising
target in CRC resistance to PDT treatment.