asking for editing, emergent, thanks, mates

5-Fu has been the golden standard of colon cancer therapy. for ages, albeit

Primary and secondary drug resistances have been the main hurdles to improving the chemotherapy efficacy.

Based on our research, in CRC RKO with deficient microRNA-21, minimised 5-Fu resistance showed that microRNA-21 is one of the main culprit to blame. (This makes no sense)

Theoretically, agents down-regulating the miR-21 expression level could be applied to restrain  can be given to restrict the development of drug resistance.

MiR-21 has been regarded as an oncogenic contributor and may play a role in 5-fu drug resistance for ages. How come does miR-21 conducts its oncogenic functions?

Many researchers have come up with various theories of mechanisms which are associated with this process.

The main attention was paid to target genes of miR-21. A number of studies showed that low PTEN expression level induced trastuzumad resistance by reinforcing its downstream PI3K/AKT phosphorylation in HER2+ cancer cells;(new sentence)

Bcl-2 over expression owning due to miR-21 high level in breast cancer plays an important part in and 5-fu resistance were also reported.

However, only few researches studies emphasised the importance of 5-Fu drug resistance induced by microRNA-21. We found that over-expression of miR-21 in CRC RKO caused decreased expression of caspase-8 even treated with 5-Fu in advance.

A possible solution to increase the sensitivity of chemotherapy can be co-treatment. A vitamin D analog called PRI-2205(5,6-trans calcipotriol) combined with 5-fluorouracil in human HT-29 colon cancer treatment was of use to reduce the chemo-resistance induced by alone lone 5-Fu-based treatment.

Another study showed that co-treatment of breast cells with topotecan and anti-miR-21 sensitises the tumor cells to anticancer drugs.

Is it 5-Fu or 5-fu? Is it microRNA-21 or miR-21? You need to be consistent in the use of abbreviations.

(My brain hurts after correcting this!)